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1. Handedness and gender influence blood pressure in young healthy men and women: A pilot study

Author

Rueda I, Banegas I, Prieto I, Wangensteen R, Segarra AB, Villarejo AB, De Gasparo M, Luna JD, Vives F, Ruiz-Bailen M, and Ramirez-Sanchez M

Subjects
brain asymmetry, handedness, sex hormones, blood pressure, Diseases of the endocrine glands. Clinical endocrinology, RC648-665
Abstract

Objective. The type and level of sex steroids influence blood pressure (BP). It has been suggested that functional brain asymmetries may be influenced by sex hormones. In addition, there are inter-arm differences in BP not yet related with handedness. In this study, we hypothesize a possible association between sex hormones, handedness, and inter-arm differences in blood pressure.

Published
2016
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2. ESICM LIVES 2016: part two: Milan, Italy. 1–5 October 2016

Author

Sivakumar, S., Taccone, F. S., Desai, K. A., Lazaridis, C., Skarzynski, M., Sekhon, M., Henderson, W., Griesdale, D., Chapple, L., Deane, A., Williams, L., Strickland, R., Lange, K., Heyland, D., Chapman, M., Rowland, M. J., Garry, P., Westbrook, J., Corkill, R., Antoniades, C. A., Pattinson, K. T., Fatania, G., Strong, A. J., Myers, R. B., Lazaridis, C., Jermaine, C. M., Robertson, C. S., Rusin, C. G., Hofmeijer, J., Sondag, L., Tjepkema-Cloostermans, M. C., Beishuizen, A., Bosch, F. H., van Putten, M. J. A. M., Carteron, L., Patet, C., Solari, D., Oddo, M., Ali, M. A., Dias, C., Almeida, R., Vaz-Ferreira, A., Silva, J., Monteiro, E., Cerejo, A., Rocha, A. P., Elsayed, A. A., Abougabal, A. M., Beshey, B. N., Alzahaby, K. M., Pozzebon, S., Ortiz, A. Blandino, Cristallini, S., Lheureux, O., Brasseur, A., Vincent, J. L., Creteur, J., Taccone, F. S., Hravnak, M., Yousef, K., Chang, Y., Crago, E., Friedlander, R. M., Abdelmonem, S. A., Tahon, S. A., Helmy, T. A., Meligy, H. S., Puig, F., Dunn-Siegrist, I., Pugin, J., Gupta, S., Govil, D., Srinivasan, S., Patel, S. J., N, J. K., Gupta, A., Tomar, D. S., Shafi, M., Harne, R., Arora, D. P., Talwar, N., Mazumdar, S., Papakrivou, E. E., Makris, D., Manoulakas, E., Tsolaki, B., Karadodas, B., Zakynthinos, E., Garcia, I. Palacios, Martin, A. Diaz, Encinares, V. Sanchez, Ibañez, M. Pachón, Montero, J. Garnacho, Labrador, G., Cangueiro, T. Cebrero, Poulose, V., Koh, J., Kam, J. W., Yeter, H., Kara, A., Aktepe, O., Topeli, A., Tsolakoglou, I., Intas, G., Stergiannis, P., Kolaros, A. A., Chalari, E., Athanasiadou, E., Martika, A., Fildisis, G., Faivre, V., Mengelle, C., Favier, B., Payen, D., Poppe, A., Winkler, M. S., Mudersbach, E., Schreiber, J., Wruck, M. L., Schwedhelm, E., Kluge, S., Zöllner, C., Tavladaki, T., Spanaki, A. M., Dimitriou, H., Kondili, E., Choulaki, C., Meleti, E., Kafetzopoulos, D., Georgopoulos, D., Briassoulis, G., la Torre, A. García-de, de la Torre-Prados, M. V., Tsvetanova-Spasova, T., Nuevo-Ortega, P., Rueda-Molina, C., Fernández-Porcel, A., Camara-Sola, E., Salido-Díaz, L., García-Alcántara, A., Tavladaki, T., Spanaki, A. M., Dimitriou, H., Kondili, E., Choulaki, C., Meleti, D. E., Kafetzopoulos, D., Georgopoulos, D., Briassoulis, G., Suberviola, B., Riera, J., Rellan, L., Sanchez, M., Robles, J. C., Lopez, E., Vicente, R., Miñambres, E., Santibañez, M., Le Guen, M., Moore, J., Mason, N., Windpassinger, M., Plattner, O., Mascha, E., Sessler, D. I., Research, Outcomes, Melia, U., Fontanet, J., van den Berg, J. P., Struys, M. M. R. F., Vereecke, H. E. M., Jensen, E. W., Rood, P. J. T., van de Schoor, F., van Tertholen, K., Pickkers, P., van den Boogaard, M., Beardow, Z. J., Redhead, H., Paramasivam, K., Numan, T., van den Boogaard, M., Kamper, A. M., Rood, P., Peelen, L. M., Zeman, P. M., Slooter, A. J., van Ewijk, C. E., Jacobs, G. E., Girbes, A. R. J., Myatra, S. N., Harish, M. M., Prabu, N. R., Siddiqui, S., Kulkarni, A. P., Divatia, J. V., Murbach, L. D., Leite, M. A., Osaku, E. F., Costa, C. R. L. M., Pelenz, M., Neitzke, N. M., Moraes, M. M., Jaskowiak, J. L., Silva, M. M. M., Zaponi, R. S., Abentroth, L. R. L., Ogasawara, S. M., Jorge, A. C., Duarte, P. A. D., Hernández-Sánchez, N., Sánchez-Hurtado, L. A., García-Guillen, F. J., Ñamendys-Silva, S. A., Maghsoudi, B., Emami, M., Khosravi, M. B., Zand, F., Tabatabaie, H. R., Masjedi, M., Sabetiyan, G., Mokri, A., Troubleyn, J., Diltoer, M., Jacobs, R., Nguyen, D. N., De Waele, E., De Regt, J., Honoré, P. M., Van Gorp, V., Spapen, H. D., Contreras, R. S., Toapanta, N. D., Moreno, G., Sabater, J., Torrado, H., Gonzalez, M., Marin, M., Farigola, E., Gonzalez, A., Fernandez, J., Vera, A., Gisbert, X., Juliá, C., Uya, J., Corral, L., Elias-Jones, I., Gemmell, L., MacKay, A., Randall, D., Adwaney, A., Blunden, M., Prowle, J. R., Kirwan, C. J., Thomas, N., Martin, A., Owen, H., Darwin, L., Conway, D., Atkinson, D., Sharman, M., Moore, J., Barbanti, C., Amour, J., Gaudard, P., Rozec, B., Mauriat, P., M’rini, M., Leger, P. L., Cambonie, G., Liet, J. M., Girard, C., Laroche, S., Damas, P., Assaf, Z., Loron, G., Lecourt, L., Pouard, P., Randall, D., Adwaney, A., Blunden, M., Prowle, J.R., Kirwan, C. J., Kim, S. H., Na, S., Kim, J., Oh, S. Y., Jung, C. W., Yoo, S. H., Min, S. H., Chung, E. J., Lee, H., Lee, N. J., Lee, K. W., Suh, K. S., Ryu, H. G., Marshall, D. C., Goodson, R. J., Salciccioli, J. D., Shalhoub, J., Potter, E. K., Kirk-Bayley, J., Karanjia, N. D., Forni, L. G., Creagh-Brown, B. C., Bossy, M., Nyman, M., Tailor, A., Creagh-Brown, B., D’Antini, D., Spadaro, S., Valentino, F., Sollitto, F., Cinnella, G., Mirabella, L., Calvo, F. J. Redondo, Bejarano, N., Padilla, D., Baladron, V., Villajero, P., Villazala, R., Redondo, J., Yuste, A. S., Liu, J., Shen, F., Teboul, J. L., Anguel, N., Beurton, A., Bezaz, N., Richard, C., Monnet, X., Fossali, T., Colombo, R., Ottolina, D., Rossetti, M., Mazzucco, C., Marchi, A., Porta, A., Catena, E., Tollisen, K. H., Andersen, G. Ø., Heyerdahl, F., Jacobsen, D., de Waard, M. C., Girbes, A. R. J., van IJzendoorn, M. C. O., Buter, H., Kingma, W. P., Navis, G. J., Boerma, E. C., Rulisek, J., Balik, M., Zacharov, S., Kim, H. S., Jeon, S. J., Namgung, H., Lee, E., Lee, E., Cho, Y. J., Lee, Y. J., Huang, A., Cioccari, L., Luethi, N., Mårtensson, J., Bellomo, R., Forsberg, M., Edman, G., Höjer, J., Forsberg, S., Freile, M. T. Chiquito, Hidalgo, F. N., Molina, J. A. Martinez, Lecumberri, R., Rosselló, A. Figuerola, Travieso, P. Medrano, Leon, G. Tuero, Sanchez, J. Gonzalez, Frias, L. Sahuquillo, Rosello, D. Balsells, Verdejo, J. A. Garcia, Serrano, J. A. Noria, Winterwerp, D., van Galen, T., Vazin, A., Karimzade, I., Zand, A., Ozen, E., Ekemen, S., Akcan, A., Sen, E., Yelken, B. Buyukkidan, Kureshi, N., Fenerty, L., Thibault-Halman, G., Erdogan, M., Walling, S., Green, R. S., Clarke, D. B., Briassoulis, P., Kalimeris, K., Ntzouvani, A., Nomikos, T., Papaparaskeva, K., Politi, E., Kostopanagiotou, G., Crewdson, K., Rehn, M., Weaver, A., Brohi, K., Lockey, D., Wright, S., Thomas, K., Baker, C., Mansfield, L., Stafford, V., Wade, C., Watson, G., Bryant, A., Chadwick, T., Shen, J., Wilkinson, J., Furneval, J., Henderson, A., Hugill, K., Howard, P., Roy, A., Bonner, S., Baudouin, S., Ramírez, C. Sánchez, Escalada, S. Hípola, Viera, M. A. Hernández, Santana, M. Cabrera, Balcázar, L. Caipe, Monroy, N. Sangil, Campelo, F. Artiles, Vázquez, C. F. Lübbe, Santana, P. Saavedra, Santana, S. Ruiz, Carteron, L., Patet, C., Quintard, H., Solari, D., Bouzat, P., Oddo, M., Wollersheim, T., Malleike, J., Haas, K., Carbon, N., Schneider, J., Birchmeier, C., Fielitz, J., Spuler, S., Weber-Carstens, S., Enseñat, L., Pérez-Madrigal, A., Saludes, P., Proença, L., Gruartmoner, G., Espinal, C., Mesquida, J., Huber, W., Eckmann, M., Elkmann, F., Gruber, A., Lahmer, T., Mayr, U., Herner, A., Schellnegger, R., Schneider, J., Schmid, R. M., Ayoub, W., Samy, W., Esmat, A., Battah, A., Mukhtar, S., Mongkolpun, W., Cortés, D. Orbegozo, Cordeiro, C. P. R., Vincent, J. L., Creteur, J., Funcke, S., Groesdonk, H., Saugel, B., Wagenpfeil, G., Wagenpfeil, S., Reuter, D. A., Fernandez, M. M., Fernandez, R., Magret, M., González-Castro, A., Bouza, M. T., Ibañez, M., García, C., Balerdi, B., Mas, A., Arauzo, V., Añón, J. M., Ruiz, F., Ferreres, J., Tomás, R., Alabert, M., Tizón, A. I., Altaba, S., Llamas, N., Goligher, E C., Fan, E., Herridge, M., Vorona, S., Sklar, M., Dres, M., Rittayamai, N., Lanys, A., Urrea, C., Tomlinson, G., Reid, W. D., Rubenfeld, G. D., Kavanagh, B. P., Brochard, L. J., Ferguson, N. D., Neto, A. Serpa, de Abreu, M. Gama, Pelosi, P., Schultz, M. J., Guérin, C., Papazian, L., Reignier, J., Ayzac, L., Loundou, A., Forel, J. M., Rolland-Debord, C., Bureau, C., Poitou, T., Clavel, M., Perbet, S., Terzi, N., Kouatchet, A., Similowski, T., Demoule, A., Hunfeld, N., Trogrlic, Z., Ladage, S., Osse, R. J., Koch, B., Rietdijk, W., Devlin, J., van der Jagt, M., Picetti, E., Ceccarelli, P., Mensi, F., Malchiodi, L., Risolo, S., Rossi, I., Antonini, M. V., Servadei, F., Caspani, M. L., Roquilly, A., Lasocki, S., Seguin, P., Geeraerts, T., Perrigault, P. F., Dahyot-Fizelier, C., Paugam-Burtz, C., Cook, F., Cinotti, R., dit Latte, D. Demeure, Mahe, P. J., Fortuit, C., Feuillet, F., Asehnoune, K., Marzorati, C., Spina, S., Scaravilli, V., Vargiolu, A., Riva, M., Giussani, C., Sganzerla, E., Citerio, G., Barbadillo, S., de Molina, F. J. González, Álvarez-Lerma, F., Rodríguez, A., Zakharkina, T., Martin-Loeches, I., Matamoros, S., Povoa, P., Torres, A., Kastelijn, J., Hofstra, J. J., de Jong, M., Schultz, M., Sterk, P., Artigas, A., Bos, L. J., Moreau, A. S., Martin-Loeches, I., Povoa, P., Salluh, J., Rodriguez, A., Nseir, S., de Jong, E., van Oers, J. A., Beishuizen, A., Girbes, A. R. J., Nijsten, M. W. N., de Lange, D. W., Bonvicini, D., Labate, D., Benacchio, L., Olivieri, A., Pizzirani, E., Lopez-Delgado, J. C., Gonzalez-Romero, M., Fuentes-Mila, V., Berbel-Franco, D., Romera-Peregrina, I., Martinez-Pascual, A., Perez-Sanchez, J., Abellan-Lencina, R., Ávila-Espinoza, R. E., Moreno-Gonzalez, G., Sbraga, F., Griffiths, S., Grocott, M. P. W., Creagh-Brown, B., Doyle, J., Wilkerson, P., Soon, Y., Huddart, S., Dickinson, M., Riga, A., Zuleika, A., Miyamoto, K., Kawazoe, Y., Morimoto, T., Yamamoto, T., Fuke, A., Hashimoto, A., Koami, H., Beppu, S., Katayama, Y., Ito, M., Ohta, Y., Yamamura, H., Rygård, S. L., Holst, L B., Wetterslev, J., Johansson, P. I., Perner, A., Soliman, I. W., de Lange, D. W., van Dijk, D., van Delden, J. J. M., Cremer, O. L., Slooter, A. J. C., Peelen, L. M., McWilliams, D., Snelson, C., Neves, A. Das, Loudet, C. I., Busico, M., Vazquez, D., Villalba, D., Veronesi, M., Lischinsky, A., López, F. J. L., Mori, L. Benito, Plotnikow, G., Díaz, A., Giannasi, S., Hernandez, R., Krzisnik, L., Cecotti, C., Viola, L., Lopez, R., Sottile, J. P., Benavent, G., Estenssoro, E., Chen, C. M., Lai, C. C., Cheng, K. C., Chou, W., Chan, K. S., Roeker, L. E., Horkan, C. M., Gibbons, F. K., Christopher, K. B., Weijs, P. J. M., Mogensen, K. M., Rawn, J. D., Robinson, M. K., Christopher, K. B., Tang, Z., Qiu, C., Ouyang, B., Cai, C., Guan, X., Regueira, T., Cea, L., Carlos, S. Juan, Elisa, B., Puebla, C., Vargas, A., Poulsen, M. K., Thomsen, L. P., Kjærgaard, S., Rees, S. E., Karbing, D. S., Wollersheim, T., Frank, S., Müller, M. C., Carbon, N. M., Skrypnikov, V., Pickerodt, P. A., Falk, R., Mahlau, A., Weber-Carstens, S., Lee, A., Inglis, R., Morgan, R., Barker, G., Kamata, K., Abe, T., Saitoh, D., Tokuda, Y., Green, R. S., Butler, M. B., Erdogan, M., Hwa, H. Tae, Gil, L. Jae, Vaquero, R. Hernández, Rodriguez-Ruiz, E., Lago, A. Lopez, Allut, J. L. Garcia, Gestal, A. Estany, Gonzalez, M. A. Garcia, Thomas-Rüddel, D. O., Schwarzkopf, D., Fleischmann, C., Reinhart, K., Suwanpasu, S., Sattayasomboon, Y., Filho, N. M. Filgueiras, Oliveira, J. C. A., Ballalai, C. S., De Lucia, C. V., Araponga, G. P., Veiga, L. N., Silva, C. S., Garrido, M. E., Ramos, B. B., Ricaldi, E. F., Gomes, S. S., Gemmell, L., MacKay, A., Wright, C., Docking, R. I., Doherty, P., Black, E., Stenhouse, P., Plummer, M. P., Finnis, M. E., Phillips, L. K., Kar, P., Bihari, S., Biradar, V., Moodie, S., Horowitz, M., Shaw, J. E., Deane, A. M., Yatabe, T., Inoue, S., Sakaguchi, M., Egi, M., Abdelhamid, Y. Ali, Plummer, M. P., Finnis, M. E., Phillips, L. K., Kar, P., Bihari, S., Biradar, V., Moodie, S., Horowitz, M., Shaw, J. E., Deane, A. M., Hokka, M., Egi, M., Mizobuchi, S., Kar, P., Plummer, M., Abdelhamid, Y. Ali, Giersch, E., Summers, M., Hatzinikolas, S., Heller, S., Chapman, M., Jones, K., Horowitz, M., Deane, A., Schweizer, R., Jacquet-Lagreze, M., Portran, P., Junot, S., Allaouchiche, B., Fellahi, J. L., Guerci, P., Ergin, B., Kapucu, A., Ince, C., Cioccari, L., Luethi, N., Crisman, M., Bellomo, R., Mårtensson, J., Shinotsuka, C. Righy, Fagnoul, D., Brasseur, A., Orbegozo, D., Vincent, J. L., Preiser, J. C., Preiser, J. C., Lheureux, O., Thooft, A., Brimioulle, S., Vincent, J. L., Iwasaka, H., Tahara, S., Nagamine, M., Ichigatani, A., Cabrera, A. Rugerio, Zepeda, E. Monares, Granillo, J. Franco, Sánchez, J. S. Aguirre, Montoya, A. A. Tanaka, Montenegro, A. Pedraza, Blanco, G. A. Gálvez, Robles, C. M. Coronado, Drolz, A., Horvatits, T., Roedl, K., Rutter, K., Kluge, S., Funk, G. C., Schneeweiss, B., Fuhrmann, V., Sabetian, G., Pooresmaeel, F., Zand, F., Ghaffaripour, S., Farbod, A., Tabei, H., Taheri, L., Anandanadesan, R., Metaxa, V., Teixeira, C., Pereira, S. M., Hernández-Marrero, P., Carvalho, A. S., Beckmann, M., Hartog, C. S., Schwarzkopf, D., Raadts, A., Robertsen, A., Førde, R., Skaga, N. O., Helseth, E., Honeybul, S., Ho, K., Lopez, P. Martinez, Gonzalez, M. Nieto, Ortega, P. Nuevo, Sola, E. Camara, Spasova, T., de la Torre-Prados, M. V., Kopecky, O., Rusinova, K., Waldauf, P., Cepeplikova, Z., Balik, M., Domínguez, J. Palamidessi, Almudevar, P. Matia, Carmona, S. Alcántara, Muñoz, J. J. Rubio, Castañeda, D. Palacios, Abellán, A. Naharro, Villamizar, P. Rodríguez, Ramos, J. Veganzones, Pérez, L. Pérez, Lucendo, A. Pérez, Ejarque, M. Camós, Estella, A., Camps, V. Lopez, Martín, M. C., Masnou, N., Barbosa, S., Varela, A., Palma, I., Cristina, L., Nunes, E., Pereira, I., Campello, G., Granja, C., Pande, R., Pandey, M., Varghese, S., Chanu, M., Van Dam, M. J., Ter Braak, E. W. M. T., Estella, A., Gracia, M., Viciana, R., Recuerda, M., Fontaiña, L. Perez, Tharmalingam, B., Kovari, F., Rose, L., Mcginlay, M., Amin, R., Burns, K., Connolly, B., Hart, N., Jouvet, P., Katz, S., Leasa, D., Mawdsley, C., Mcauley, D., Schultz, M., Blackwood, B., Denham, S., Worrall, R., Arshad, M., Isherwood, P., Khadjibaev, A., Sabirov, D., Rosstalnaya, A., Parpibaev, F., Sharipova, V., Blanco, G. A. Galvez, Guzman, C. I. Olvera, Sánchez, J. S. Aguirre, Granillo, J. Franco, Gupta, S., Govil, D., Srinivasan, S., Patel, S. J., N, J. K., Gupta, A., Shafi, M., Tomar, D. S., Harne, R., Arora, D. P., Talwar, N., Mazumdar, S., Cha, Y. S., Lee, S. J., Tyagi, N., Rajput, R. K., Taneja, S., Singh, V. K., Sharma, S. C., Mittal, S., Rao, B. K., Ayachi, J., Fraj, N., Romdhani, S., Khedher, A., Meddeb, K., Sma, N., Azouzi, A., Bouneb, R., Chouchene, I., El Ghardallou, M., Boussarsar, M., Jennings, R., Walter, E., Ribeiro, J. M., Moniz, I., Marçal, R., Santos, A. C., Candeias, C., e Silva, Z. Costa, Gomez, S. E. Zamora, Nieto, O. R. Perez, Gonzalez, J. A. Castanon, Cuellar, A. I. Vasquez, Mildh, H., Pettilä, V., Korhonen, A. M., Karlsson, S., Ala-Kokko, T., Reinikainen, M., Vaara, S. T., Zaleska-Kociecka, M., Grabowski, M., Dąbrowski, M., Wozniak, S., Piotrowska, K., Banaszewski, M., Imiela, J., Stepinska, J., Pérez, A. González, Ordoñez, P. Florez, Giribet, A., Cuervo, M. A. Alonso, Cuervo, R. Alonso, Esteban, M. A. Rodriguez, Fraile, L. Iglesias, Mittelbrum, C. Ponte, Albaiceta, G. Muñiz, Koeze, J., Keus, F., Dieperink, W., van der Horst, I. C. C., van Meurs, M., Zijlstra, J. G., Roberts, S., Caballero, C. 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C., Vieira, Jr, J. M., Azevedo, L. C. P., Nurses of the Central and General ICUs of Shiraz Namazi Hospital, Sedation an Delirium Group Hospital Universitari de Bellvitge, SPACeR group (Surrey Peri-operative, Anaesthesia and Critical Care Collaborative Research Group), for the PRoVENT investigators and the PROVE Network, SEMICYUC/GETGAG Working Group, TAVeM study group, POPC-CB investigators, DESIRE (DExmedetomidine for Sepsis in ICU Randomized Evaluation) Trial Investigators, GEMINI, Bioethics work group of SEMICYUC, The FINNAKI Study Group, Queen Square Neuroanaesthesia and Neurocritical Care Resreach Group, Renal Transplantation HUVR, GEMINI, EDISVAL Group, EDISVAL Group, PLUG Working group, TAVeM study Group, The FINNAKI Study Group, on behalf of Department of Professional Development, ESICM, Critical Care Research Group, SIRAKI group, and Grupo ESBAGA

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2016
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5. Intracerebral hemorrhage in ICU: is it worth treating?

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Sivakumar, S, Taccone, F, Desai, K, Lazaridis, C, Skarzynski, M, Sekhon, M, Henderson, W, Griesdale, D, Chapple, L, Deane, A, Williams, L, Strickland, R, Lange, K, Heyland, D, Chapman, M, Rowland, M, Garry, P, Westbrook, J, Corkill, R, Antoniades, C, Pattinson, K, Fatania, G, Strong, A, Myers, R, Jermaine, C, Robertson, C, Rusin, C, Hofmeijer, J, Sondag, L, Tjepkema Cloostermans, M, Beishuizen, A, Bosch, F, van Putten, M, Carteron, L, Patet, C, Solari, D, Oddo, M, Ali, M, Dias, C, Almeida, R, Vaz Ferreira, A, Silva, J, Monteiro, E, Cerejo, A, Rocha, A, Elsayed, A, Abougabal, A, Beshey, B, Alzahaby, K, Pozzebon, S, Ortiz, A, Cristallini, S, Lheureux, O, Brasseur, A, Vincent, J, Creteur, J, Hravnak, M, Yousef, K, Chang, Y, Crago, E, Friedlander, R, Abdelmonem, S, Tahon, S, Helmy, T, Meligy, H, Puig, F, Dunn Siegrist, I, Pugin, J, Gupta, S, Govil, D, Srinivasan, S, Patel, S, N, J, Gupta, A, Tomar, D, Shafi, M, Harne, R, Arora, D, Talwar, N, Mazumdar, S, Papakrivou, E, Makris, D, Manoulakas, E, Tsolaki, B, Karadodas, B, Zakynthinos, E, Garcia, I, Martin, A, Encinares, V, Ibañez, M, Montero, J, Labrador, G, Cangueiro, T, Poulose, V, Koh, J, Kam, J, Yeter, H, Kara, A, Aktepe, O, Topeli, A, Tsolakoglou, I, Intas, G, Stergiannis, P, Kolaros, A, Chalari, E, Athanasiadou, E, Martika, A, Fildisis, G, Faivre, V, Mengelle, C, Favier, B, Payen, D, Poppe, A, Winkler, M, Mudersbach, E, Schreiber, J, Wruck, M, Schwedhelm, E, Kluge, S, Zöllner, C, Tavladaki, T, Spanaki, A, Dimitriou, H, Kondili, E, Choulaki, C, Meleti, E, Kafetzopoulos, D, Georgopoulos, D, Briassoulis, G, la Torre, A, de la Torre Prados, M, Tsvetanova Spasova, T, Nuevo Ortega, P, Rueda Molina, C, Fernández Porcel, A, Camara Sola, E, Salido Díaz, L, García Alcántara, A, Meleti, D, Suberviola, B, Riera, J, Rellan, L, Sanchez, M, Robles, J, Lopez, E, Vicente, R, Miñambres, E, Santibañez, M, Le Guen, M, Moore, J, Mason, N, Windpassinger, M, Plattner, O, Mascha, E, Sessler, D, Research, O, Melia, U, Fontanet, J, 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Laisne, L, Rabbat, A, Lebert, C, Perez, P, Chaize, M, Renault, A, Meert, A, Hamidfar, R, Jourdain, M, Darmon, M, Schlemmer, B, Chevret, S, Lemiale, V, Azoulay, E, Benoit, D, Martins Branco, D, Sousa, M, Marum, S, Bouw, M, Galstyan, G, Makarova, P, Parovichnikova, E, Kuzmina, L, Troitskaya, V, Drize, N, Gemdzhian, E, Savchenko, V, Chao, H, Kılıc, E, Demiriz, B, Uygur, M, Sürücü, M, Cınar, K, Yıldırım, A, Kiss, K, Köves, B, Csernus, V, Molnár, Z, Ntantana, A, Matamis, D, Savvidou, S, Giannakou, M, Gouva, M, Nakos, G, Koulouras, V, Gaffney, S, Judge, C, Drew, T, Misran, H, Munshi, R, Mcgovern, L, Coyle, M, Dunne, L, Deasy, E, Lavin, P, Fahy, A, Darcy, D, Donnelly, M, Ismail, N, Hall, T, Wykes, K, Jack, J, Ngu, W, Morgan, P, Ruiz Ramos, J, Ramirez, P, Gordon, M, Villarreal, E, Frasquet, J, Poveda Andrés, J, Castellanos, A, Ijssennagger, C, Ten Hoorn, S, van Wijk, A, van den Broek, J, Tuinman, P, Elmenshawy, A, Hammond, B, Gibbon, G, Belcham, T, Burton, K, Taniguchi, L, Ramos, F, Momma, A, 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Rosenqvist, M, Melander, O, Chew, M, Kishihara, Y, Yasuda, H, Jimenez, R, Torrella, P, Fernandez, A, Sanchez, S, Ortin, A, Prats, R, Aguilera, E, Marti, D, Fernandez, L, Ferrer, M, Lanziotti, V, Pulcheri, L, Ribeiro, M, Barbosa, A, E. Silva, J, Soares, M, Marqués, M, Moreno, A, Pizarraya, A, Smani, Y, Connell, M, Zhang, L, Parker, R, Banerjee, I, Clermont, G, Norberg, E, Oras, J, Cuisinier, A, Maufrais, C, Payen, J, Nottin, S, Walther, G, Arib, S, Bilotta, F, Badenes, R, Rubulotta, F, Mirek, S, Monfort, B, Stazi, E, Roig, A, Magnoni, S, Marando, M, Pifferi, S, Conte, V, Ortolano, F, Carbonara, M, Bertani, G, Scola, E, Cadioli, M, Triulzi, F, Colombo, A, Stocchetti, N, Rotzel, H, Lázaro, A, Prada, D, Guimillo, M, Piqueras, C, Guia, J, Simon, M, Arizmendi, A, Carratalá, A, El Maraghi, S, Yehia, A, Bakry, M, Shoman, A, Backes, F, Bianchin, M, Vieira, S, de Souza, A, Backes, A, Klein, C, Arunkumar, A, Lozano, A, Gallaher, C, Cattlin, S, Gordon, S, Picard, J, Fontana, V, Bond, O, Nobile, L, Mrozek, S, Delamarre, L, Capilla, F, Al Saati, T, Fourcade, O, Dominguez Berrot, A, Gonzalez Vaquero, M, Vallejo Pascual, M, Gupta, D, Ivory, B, Chopra, M, Mccarthy, J, Felderhof, C, Macneil, C, Maggiorini, M, Duska, F, Fumis, R, Junior, J, Amarante, G, Skorko, A, Sanders, S, Aron, J, Kroll, R, Redfearn, C, Krishnan, P, Khalil, J, Kongpolprom, N, Gulia, V, Lourenço, E, Duro, C, Baptista, G, Alves, A, Arminda, B, Rodrigues, M, Hayward, J, Baldwin, F, Gray, R, Katinakis, P, Stijf, M, Ten Kleij, M, Jansen Frederiks, M, Broek, R, de Bruijne, M, Spronk, P, Sinha, K, Luney, M, Palmer, K, Keating, L, Abu Habsa, M, Bahl, R, Baskaralingam, N, Ahmad, A, Kanapeckaite, L, Bhatti, P, Glace, S, Jeyabraba, S, Lewis, H, Kostopoulos, A, Raja, M, West, A, Ely, A, Turkoglu, L, Zolfaghari, P, Baptista, J, Marques, M, Martins, P, Pimentel, J, Su, Y, Villacres, S, Stone, M, Parsikia, A, Medar, S, O'Dea, K, Porter, J, Tirlapur, N, Jonathan, J, Singh, S, Takata, M, Mcwhirter, E, Lyon, R, Hariz, M, Azmi, E, Alkhan, J, Movsisyan, V, Petrikov, S, Marutyan, Z, Aliev, I, Evdokimov, A, Antonucci, E, Merz, T, Hartmann, C, Calzia, E, Radermacher, P, Nußbaum, B, Huber Lang, M, Gröger, M, Svoren Jabalera, E, Davenport, E, Humburg, P, Knight, J, Hinds, C, Jun, I, Kim, W, Besch, G, Perrotti, A, Puyraveau, M, Baltres, M, Samain, E, Chocron, S, Pili Floury, S, Plata Menchaca, E, Sabater Riera, J, Estruch, M, Boza, E, Toscana Fernández, J, Bruguera Pellicer, E, Ordoñez Llanos, J, Pérez Fernández, X, Cavaleiro, P, Tralhão, A, Arrigo, M, Lopes, J, Lebrun, M, Cholley, B, Perezvela, J, Marinmateos, H, Rivera, J, Llorente, M, De Marcos, B, Fernandez, F, Laborda, C, Zamora, D, Delgado, J, Imperiali, C, Dastis, M, Górka, J, Górka, K, Iwaniec, T, Frołow, M, Polok, K, Fronczek, J, Kózka, M, Musiał, J, Szczeklik, W, Sileli, M, Moursia, C, Maleoglou, H, Leleki, K, Uz, Z, Ince, Y, Papatella, R, Bulent, E, De Mol, B, Vicka, V, Gineityte, D, Ringaitiene, D, Norkiene, I, Sipylaite, J, Möller, C, Thomas Rueddel, D, Vlasakov, V, Rochwerg, B, Theurer, P, Al Sibai, J, Camblor, P, Fernandez, P, Gala, J, Guisasola, J, Tamura, T, Miyajima, I, Yamashita, K, Yokoyama, M, Dalampini, E, Nastou, M, Baddour, A, Ignatiadis, A, Asteri, T, Hathorn, K, Purtle, S, Viana, M, Tonietto, T, Gross, L, Costa, V, Tavares, A, Lisboa, B, Moraes, R, Viana, L, Azevedo, M, Ceniccola, G, Pequeno, R, Holanda, T, Mendonça, V, Araújo, W, Carvalho, L, Segaran, E, Vickers, L, Brinchmann, K, Wignall, I, De Brito Ashurst, I, Del Olmo, R, Vaquerizo, C, Carreño, R, Gálvez, V, Kaminsky, G, Nieto, B, Fuentes, M, De la Torre, M, Torres, E, Alonso, A, Velayos, C, Saldaña, T, Escribá, A, Grip, J, Kölegård, R, Sundblad, P, Rooyackers, O, Naser, B, Jaziri, F, Jazia, A, Barghouth, M, Hentati, O, Skouri, W, El Euch, M, Mahfoudhi, M, Turki, S, Abdelghni, K, Abdallah, B, Maha, B, Lorente, M, Włudarczyk, A, Hałek, A, Bargouth, M, Bennasr, M, Abdelghani, K, Abdallah, T, Geenen, I, Parienti, J, Shum, H, King, H, Yan, W, Londoño, J, Cardenas, C, Pedrosa, M, Gubianas, C, Bertolin, C, Batllori, N, Sirvent, J, Mukhopadhyay, A, Chan, H, Kowitlawakul, Y, Remani, D, Leong, C, Henry, C, Puthucheary, Z, Mendsaikhan, N, Begzjav, T, Lundeg, G, Dünser, M, Welsh, S, Guerra, E, Zerpa, M, Zechner, F, Berdaguer, F, Risso Vazquez, A, Masevicius, F, Greaney, D, Magee, A, Fitzpatrick, G, Lugo Cob, R, Tejeda Huezo, B, Cano Oviedo, A, Aydogan, M, Togal, T, Taha, A, Chai, H, Kam, C, Razali, S, Sivasamy, V, Kuan, L, Morales, M, Pires, T, and Azevedo, L

Subjects
intracerebral haemorrhage in intensive care
Published
2016

6. ESICM LIVES 2016: part two

Author

Sivakumar, S., Taccone, F. S., Desai, K. A., Lazaridis, C., Skarzynski, M., Sekhon, M., Henderson, W., Griesdale, D., Chapple, L., Deane, A., Williams, L., Strickland, R., Lange, K., Heyland, D., Chapman, M., Rowland, M. J., Garry, P., Westbrook, J., Corkill, R., Antoniades, C. A., Pattinson, K. T., Fatania, G., Strong, A. J., Myers, R. B., Jermaine, C. M., Robertson, C. S., Rusin, C. G., Hofmeijer, J., Sondag, L., Tjepkema-Cloostermans, M. C., Beishuizen, A., Bosch, F. H., van Putten, M. J. A. M., Carteron, L., Patet, C., Solari, D., Oddo, M., Ali, M. A., Dias, C., Almeida, R., Vaz-Ferreira, A., Silva, J., Monteiro, E., Cerejo, A., Rocha, A. P., Elsayed, A. A., Abougabal, A. M., Beshey, B. N., Alzahaby, K. M., Pozzebon, S., Ortiz, A. Blandino, Cristallini, S., Lheureux, O., Brasseur, A., Vincent, J. L., Creteur, J., Hravnak, M., Yousef, K., Chang, Y., Crago, E., Friedlander, R. M., Abdelmonem, S. A., Tahon, S. A., Helmy, T. A., Meligy, H. S., Puig, F., Dunn-Siegrist, I., Pugin, J., Gupta, S., Govil, D., Srinivasan, S., Patel, S. J., N, J. K., Gupta, A., Tomar, D. S., Shafi, M., Harne, R., Arora, D. P., Talwar, N., Mazumdar, S., Papakrivou, E. E., Makris, D., Manoulakas, E., Tsolaki, B., Karadodas, B., Zakynthinos, E., Garcia, I. Palacios, Martin, A. Diaz, Encinares, V. Sanchez, Ibañez, M. Pachón, Montero, J. Garnacho, Labrador, G., Cangueiro, T. Cebrero, Poulose, V., Koh, J., Kam, J. W., Yeter, H., Kara, A., Aktepe, O., Topeli, A., Tsolakoglou, I., Intas, G., Stergiannis, P., Kolaros, A. A., Chalari, E., Athanasiadou, E., Martika, A., Fildisis, G., Faivre, V., Mengelle, C., Favier, B., Payen, D., Poppe, A., Winkler, M. S., Mudersbach, E., Schreiber, J., Wruck, M. L., Schwedhelm, E., Kluge, S., Zöllner, C., Tavladaki, T., Spanaki, A. M., Dimitriou, H., Kondili, E., Choulaki, C., Meleti, E., Kafetzopoulos, D., Georgopoulos, D., Briassoulis, G., la Torre, A. García-de, de la Torre-Prados, M. V., Tsvetanova-Spasova, T., Nuevo-Ortega, P., Rueda-Molina, C., Fernández-Porcel, A., Camara-Sola, E., Salido-Díaz, L., García-Alcántara, A., Meleti, D. E., Suberviola, B., Riera, J., Rellan, L., Sanchez, M., Robles, J. C., Lopez, E., Vicente, R., Miñambres, E., Santibañez, M., Le Guen, M., Moore, J., Mason, N., Windpassinger, M., Plattner, O., Mascha, E., Sessler, D. I., Research, Outcomes, Melia, U., Fontanet, J., van den Berg, J. P., Struys, M. M. R. F., Vereecke, H. E. M., Jensen, E. W., Rood, P. J. T., van de Schoor, F., van Tertholen, K., Pickkers, P., van den Boogaard, M., Beardow, Z. J., Redhead, H., Paramasivam, K., Numan, T., Kamper, A. M., Rood, P., Peelen, L. M., Zeman, P. M., Slooter, A. J., van Ewijk, C. E., Jacobs, G. E., Girbes, A. R. J., Myatra, S. N., Harish, M. M., Prabu, N. R., Siddiqui, S., Kulkarni, A. P., Divatia, J. V., Murbach, L. D., Leite, M. A., Osaku, E. F., Costa, C. R. L. M., Pelenz, M., Neitzke, N. M., Moraes, M. M., Jaskowiak, J. L., Silva, M. M. M., Zaponi, R. S., Abentroth, L. R. L., Ogasawara, S. M., Jorge, A. C., Duarte, P. A. D., Hernández-Sánchez, N., Sánchez-Hurtado, L. A., García-Guillen, F. J., Ñamendys-Silva, S. A., Maghsoudi, B., Emami, M., Khosravi, M. B., Zand, F., Tabatabaie, H. R., Masjedi, M., Sabetiyan, G., Mokri, A., Troubleyn, J., Diltoer, M., Jacobs, R., Nguyen, D. N., De Waele, E., De Regt, J., Honoré, P. M., Van Gorp, V., Spapen, H. D., Contreras, R. S., Toapanta, N. D., Moreno, G., Sabater, J., Torrado, H., Gonzalez, M., Marin, M., Farigola, E., Gonzalez, A., Fernandez, J., Vera, A., Gisbert, X., Juliá, C., Uya, J., Corral, L., Elias-Jones, I., Gemmell, L., MacKay, A., Randall, D., Adwaney, A., Blunden, M., Prowle, J. R., Kirwan, C. J., Thomas, N., Martin, A., Owen, H., Darwin, L., Conway, D., Atkinson, D., Sharman, M., Barbanti, C., Amour, J., Gaudard, P., Rozec, B., Mauriat, P., M’rini, M., Leger, P. L., Cambonie, G., Liet, J. 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Cambronero, Jiménez, R., Rebollo, S., Alejandro, O., Fernández, A., Moreno, S., Herrera, L., Ojados, A., Galindo, M., Murcia, J., Contreras, M., Sánchez-Argente, S., Bonilla, Y., Rodríguez, M. D., Allegue, J. M., Cakin, Ö., Parlak, H., Kirca, H., Mutlu, F., Aydınlı, B., Cengiz, M., Ramazanoglu, A., Jung, E.-J., Oh, S.-Y., Domenech, J. Cebrián, Montalvo, A. Pinos, Chornet, T. Ciges, Martinez, P. Concha, Ribas, M. Piñol, Costa, R. Gimeno, Ortega, A. Castellanos, Forbes, C., Prescott, H., Lal, A., Khan, F. A., Dela Pena, E. G., Dizon, J. S., Perez, P. P. P., Wong, C. M. J., Garach, M. Muñoz, Romero, O. Moreno, Puerta, R. Ramirez, Diaz, F. Acosta, Bailon, A. M. Perez, Pinel, A. Carranza, Maldonado, L. Peñas, Kalaiselvan, M. S., kumar, R. L. Siva, Renuka, M. K., Kumar, A. S. Arun, De Rosa, S., Ferrari, F., Checcacci, S. Carboni, Rigobello, A., Joannidis, M., Politi, F., Pellizzari, A., Bonato, R., Fernandez-Carmona, A., Macias-Guarasa, I., Gutierrez-Rodriguez, R., Martinez-Lopez, P., Diaz-Castellanos, M. A., Arias-Diaz, M., Aguilar-Alonso, E., Nikandish, R. N., Artemenko, V., Budnyuk, A., Bassi, G. Li, Senussi, T., Idone, F., Xiol, E. Aguilera, Travierso, C., Chiurazzi, C., Motos, A., Amaro, R., Hua, Y., Fernández-Barat, L., Ranzani, O. T., Bobi, Q., Rigol, M., Youn, A., Hwang, J. Gyung, Ossorio, M. E. Yuste, Figueira, H., Oliveira, R., Mota, A., Kamp, O., Cruciger, O., Aach, M., Kaczmarek, C., Waydhas, C., Schildhauer, T. A., Hamsen, U., Camprubí-Rimblas, M., Chimenti, L., Guillamat-Prats, R., Lebouvier, T., Bringué, J., Tijero, J., Gómez, M. N., Blanch, L., Tagliabue, G., Ji, M., Jagers, J. V. Suneby, Easton, P. A., Martins, A. M. C. R. P. F., Hong, J. Y., Shin, M. H., Park, M. S., Pomprapa, A., Hofferberth, M. B. T., Russ, M., Braun, W., Walter, M., Francis, R., Lachmann, B., Leonhardt, S., Landaverde-López, A., Canedo-Castillo, N. A., Esquivel-Chávez, A., Arvizu-Tachiquín, P. C., Baltazar-Torres, J. A., Cardoso, V., Krystopchuk, A., Castro, S., Melão, L., Firmino, S., Marreiros, A., Almaziad, S., Kubbara, A., Barnett, W., Nakity, R., Alamoudi, W., Altook, R., Tarazi, T., Fida, M., Safi, F., Assaly, R., Santini, A., Milesi, M., Maraffi, T., Pugni, P., Cavenago, M., Gattinoni, L., Protti, A., Perchiazzi, G., Borges, J. B., Bayat, S., Porra, L., Broche, L., Hedenstierna, G., Larsson, A., Roneus, A., Segelsjö, M., Vestito, M. C., Gremo, E., Nyberg, A., Castegren, M., Pikwer, A., Yoshida, T., Engelberts, D., Otulakowski, G., Katira, B., Post, M., Brochard, L., Amato, M. B. P., Koch, N., Hoellthaler, J., Mair, S., Phillip, V., Beitz, A., Baladrón, V., Villarejo, P., Steenstra, R. J., Banierink, H., Hof, J., van der Horst, I. C., Nijsten, M. W., Hoekstra, M., Sterz, F., Horvatits, K., Herkner, H., Kott, M., Zitta, K., Brandt, B., Schildhauer, C., Elke, G., Hummitzsch, L., Albrecht, M., González, L. Rey, Alonso, D. Cabestrero, Sánchez, R. de Pablo, Lucas, J. Higuera, Ferlitsch, A., Fauler, G., Trauner, M., Pischke, S., Fischer, L., Thaiss, F., Koch, M., Bangert, K., Lohse, A. W., Nashan, B., Sterneck, M., Faenza, S., Siniscalchi, A., Pierucci, E., Mancini, E., Ricci, D., Gemelli, C., Cuoghi, A., Magnani, S., Atti, M., Sotos, F., Cánovas, J., López, A., Burruezo, A., Torres, D., Herrera-Gutierrez, M. E., Barrueco-Francioni, J., Arias-Verdú, D., Lozano-Saez, R., Quesada-Garcia, G., Seller-Pérez, G., Figueiredo, A., Anzola, Y., Pereira, R., Bento, L., Lai, M., Deiana, M., Seller-Perez, G., Vardas, K., Ilia, S., Sertedaki, A., Charmadari, E., Stratakis, C. A., Briassouli, E., Goukos, D., Psarra, K., Botoula, E., Tsagarakis, S., Mageira, E., Routsi, C., Nanas, S., Campello, E., Radu, C. M., Su, H., Lam, Y. M., Willis, K., Pullar, V., Hubner, R. P., Tsang, J. L., de Guadiana-Romualdo, L. García, Rebollo-Acebes, S., Esteban-Torrella, P., Jiménez-Sánchez, R., Jiménez-Santos, E., Ortín-Freire, A., Hernando-Holgado, A., Albaladejo-Otón, M. D., Coelho, L., Rabello, L., Póvoa, P., Varis, E., Poukkanen, M., Jacob, S., Takala, J., Wilkman, E., Lundberg, O. H. M., Bergenzaun, L., Rydén, J., Rosenqvist, M., Melander, O., Chew, M. S., Kishihara, Y., Yasuda, H., Jimenez, R., Torrella, P. Esteban, Fernandez, A., Sanchez, S., Ortin, A., Prats, R. Guillamat, Aguilera, E., Marti, D., Fernandez, L., Ferrer, M., Lanziotti, V. S., Pulcheri, L., Ribeiro, M. O., Barbosa, A. P., e Silva, J. R. Lapa, Soares, M., Salluh, J. I. F., Marqués, M. Gil, Moreno, A. Puppo, Pizarraya, A. Gutierrez, Diaz, J. Pachón, Smani, Y., Connell, M. Mc, Zhang, L. A., Parker, R. S., Banerjee, I., Clermont, G., Norberg, E., Oras, J., Cuisinier, A., Maufrais, C., Payen, J. F., Nottin, S., Walther, G., Arib, S., Bilotta, F., Badenes, R., Rubulotta, F., Mirek, S., Monfort, B., Stazi, E., Roig, A. Lozano, Magnoni, S., Marando, M., Pifferi, S., Conte, V., Ortolano, F., Carbonara, M., Bertani, G., Scola, E., Cadioli, M., Triulzi, F., Colombo, A., Stocchetti, N., Rotzel, H. B., Lázaro, A. Serrano, Prada, D. Aguillón, Guimillo, M. Rodriguez, Piqueras, C. Sanchís, Guia, J. Romero, Simon, M. García, Arizmendi, A. Mesejo, Carratalá, A., El Maraghi, S., Yehia, A., Bakry, M., Shoman, A., Backes, F. N., Bianchin, M. M., Vieira, S. R. R., de Souza, A., Backes, A. N., Klein, C., Arunkumar, A. S., Lozano, A., Gallaher, C., Cattlin, S., Gordon, S., Picard, J., Fontana, V., Bond, O., Nobile, L., Mrozek, S., Delamarre, L., Capilla, F., Al-Saati, T., Fourcade, O., Dominguez-Berrot, A. M., Gonzalez-Vaquero, M., Vallejo-Pascual, M. E., Gupta, D., Ivory, B. D., Chopra, M., McCarthy, J., Felderhof, C. L., MacNeil, C., Maggiorini, M., Duska, F., Fumis, R. R. L., Junior, J. M. Vieira, Amarante, G., Skorko, A., Sanders, S., Aron, J., Kroll, R. J., Redfearn, C., Krishnan, P., Khalil, J. E., Kongpolprom, N., Gulia, V., Lourenço, E., Duro, C., Baptista, G., Alves, A., Arminda, B., Rodrigues, M., Hayward, J., Baldwin, F., Gray, R., Katinakis, P. A., Stijf, M., Ten Kleij, M., Jansen-Frederiks, M., Broek, R., de Bruijne, M., Spronk, P. E., Sinha, K., Luney, M., Palmer, K., Keating, L., Abu-Habsa, M., Bahl, R., Baskaralingam, N., Ahmad, A., Kanapeckaite, L., Bhatti, P., Glace, S., Jeyabraba, S., Lewis, H. F., Kostopoulos, A., Raja, M., West, A., Ely, A., Turkoglu, L. M., Zolfaghari, P., Baptista, J. P., Marques, M. P., Martins, P., Pimentel, J., Su, Y. C., Villacres, S., Stone, M. E., Parsikia, A., Medar, S., O’Dea, K. P., Porter, J., Tirlapur, N., Jonathan, J. M., Singh, S., Takata, M., McWhirter, E., Lyon, R., Hariz, M. L., Azmi, E., Alkhan, J., Movsisyan, V., Petrikov, S., Marutyan, Z., Aliev, I., Evdokimov, A., Antonucci, E., Merz, T., Hartmann, C., Calzia, E., Radermacher, P., Nußbaum, B., Huber-Lang, M., Gröger, M., Svoren-Jabalera, E., Davenport, E. E., Humburg, P., Knight, J., Hinds, C. J., Jun, I. J., Kim, W. J., Lee, E. H., Besch, G., Perrotti, A., Puyraveau, M., Baltres, M., Samain, E., Chocron, S., Pili-Floury, S., Plata-Menchaca, E. P., Sabater-Riera, J., Estruch, M., Boza, E., Toscana-Fernández, J., Bruguera-Pellicer, E., Ordoñez-Llanos, J., Pérez-Fernández, X. L., Cavaleiro, P., Tralhão, A., Arrigo, M., Lopes, J.-P., Lebrun, M., Cholley, B., PerezVela, J. L., MarinMateos, H., Rivera, J. J. Jimenez, Llorente, M. A. Alcala, De Marcos, B. Gonzalez, Fernandez, F. J. Gonzalez, Laborda, C. Garcia, Zamora, D. Fernandez, Delgado, J. C. Lopez, Imperiali, C., Dastis, M., Górka, J., Górka, K., Iwaniec, T., Frołow, M., Polok, K., Fronczek, J., Kózka, M., Musiał, J., Szczeklik, W., Sileli, M., Moursia, C., Maleoglou, H., Leleki, K., Uz, Z., Ince, Y., Papatella, R., Bulent, E., De Mol, B., Vicka, V., Gineityte, D., Ringaitiene, D., Norkiene, I., Sipylaite, J., Möller, C., Thomas-Rueddel, D. O., Vlasakov, V., Rochwerg, B., Theurer, P., Al Sibai, J. Zanabili, Camblor, P. Martinez, Fernandez, P. Alvarez, Gala, J. M. García, Guisasola, J. Silba, Tamura, T., Miyajima, I., Yamashita, K., Yokoyama, M., Dalampini, E., Nastou, M., Baddour, A., Ignatiadis, A., Asteri, T., Hathorn, K. E., Purtle, S. W., Viana, M. V., Tonietto, T. A., Gross, L. A., Costa, V. L., Tavares, A. L. J., Lisboa, B. O., Moraes, R. B., Vieira, S. R., Viana, L. V., Azevedo, M. J., Ceniccola, G. D., Pequeno, R. S. F., Holanda, T. P., Mendonça, V. S., Araújo, W. M. C., Carvalho, L. S. F., Segaran, E., Vickers, L., Brinchmann, K., Wignall, I., De Brito-Ashurst, I., del Olmo, R., Esteban, M. J., Vaquerizo, C., Carreño, R., Gálvez, V., Kaminsky, G., Nieto, B., Fuentes, M., De la Torre, M. A., Torres, E., Alonso, A., Velayos, C., Saldaña, T., Escribá, A., GRIP, J., Kölegård, R., Sundblad, P., Rooyackers, O., Naser, Ben, Jaziri, F., Jazia, A. Ben, Barghouth, M., Hentati, O., Skouri, W., El Euch, M., Mahfoudhi, M., Turki, S., Abdelghni, K. Ben, Abdallah, Ben, Maha, B. N. M., Lorente, M., Włudarczyk, A., Hałek, A., Bargouth, M., Bennasr, M., Abdelghani, K. Ben, Abdallah, T. Ben, Geenen, I. L., Parienti, J. J., Straaten, H. M. Oudemans-van, Shum, H. P., King, H. S., Chan, K. C., Yan, W. W., Londoño, J. Gonzalez, Cardenas, C. Lorencio, Pedrosa, M. Morales, Gubianas, C. Murcia, Bertolin, C. Fuster, Batllori, N. Vila, Sirvent, J. M., Mukhopadhyay, A., Chan, H. Y., Kowitlawakul, Y., Remani, D., Leong, C. S. F., Henry, C. J., Puthucheary, Z. A., Mendsaikhan, N., Begzjav, T., Lundeg, G., Dünser, M., Welsh, S. P., Guerra, E., Zerpa, M. C. l., Zechner, F., Berdaguer, F., Risso-Vazquez, A., Masevicius, F. D., Greaney, D., Magee, A., Fitzpatrick, G., Lugo-Cob, R. G., Tejeda-Huezo, B. C., Cano-Oviedo, A. A., Aydogan, M. S., Togal, T., Taha, A., Chai, H. Z., Kam, C., Razali, S. S. Yang, Sivasamy, V., Kuan, L. Y., Morales, M. A. Lopez, Pires, T., and Azevedo, L. C. P.

Subjects
Meeting Abstracts
Abstract

Introduction In addition to systemic hemodynamics, the management\ud of neurocritically ill patients is often informed by neuromonitoring. In\ud the absence of high-level evidence clinicians are often guided by personal\ud and local expertise. Little is known about practices as they pertain\ud to the use of such monitoring in patients with acute brain injury (ABI).\ud Objectives To investigate practices in bedside monitoring for ABI patients.\ud Particularly interested in differences among “neurointensivists”\ud (NIs; defined here as intensivists whose clinical practice is comprised\ud > 1/3 by neurocritical care) and other intensivists (OIs). Also, to\ud explore patterns specific to traumatic brain injury (TBI) and subarachnoid\ud hemorrhage (SAH), as well as preferences and availability of\ud particular technologies/devices.\ud Methods Electronic survey of 22 items including two case-based scenarios;\ud endorsed by SCCM (9,000 recipients) and ESICM (on-line\ud newsletter) in 2013. A sample size of 370 was calculated based on a\ud population of 10,000 physician members, a 5 % margin error, and\ud 95 % confidence interval. We summarized results using descriptive\ud statistics (proportions with 95 % confidence intervals). A chi-square\ud test was used to compare proportions of responses between NIs and\ud OIs with a significance p < 0.05.\ud Results There were 655 responders (66 % completion rate); 422(65 %)\ud were classified as OIs and 226(35 %) as NIs. More NIs follow\ud hemodynamic protocols for neurocritically-ill patients (56 % vs. 43 %, p\ud 0.001), in TBI (44.5 % vs. 33.3 %, p 0.007), and in SAH (38.1 % vs. 21.3 %,\ud p < 000.1). For delayed cerebral ischemia (DCI), more NIs target cardiac\ud index (CI) (35 % vs. 21 %, p 0.0001), and fluid responsiveness (62 % vs.\ud 53 %, p 0.03), use more bedside ultrasound (BUS) (42 % vs. 29 %, p\ud 0.005) and arterial waveform analysis (40 % vs. 29 %, p 0.02). For DCI\ud neuromonitoring, NIs use more angiography (57 % vs. 43 %, p 0.004),\ud TCD (46 % vs. 38 %, p 0.0001), and CTP (32 % vs.16 %, p 0.0001). For\ud CPP optimization in TBI, NIs use more arterial waveform analysis (45 %\ud vs. 35 %, p 0.019), and BUS (37 % vs. 27.7 %, p 0.023), while more OIs\ud monitor mixed venous oxygen saturation (54.1 % vs. 45 %, p 0.045). For\ud TBI neuromonitoring, NIs use more PbtO2 (28 % vs. 10 %, p 0.0001). In\ud the case scenario of raised ICP/low PbtO2, most employ analgosedation\ud (47 %) and osmotherapy (38 %). Fewer make use of preserved pressure\ud reactivity, particularly OIs (vasopressor use 23 % vs. 34 %, p 0.014).\ud Conclusions There is large heterogeneity in the use of monitoring protocols,\ud variables, and technologies/devices. “Neurointensivists” not only\ud employ more neuromonitoring but also more hemodynamic monitoring\ud in patients with acute brain injury. ICP/CPP remain the most commonly\ud followed neuro-variables in TBI patients, with low use of other\ud brain-physiology parameters, sugg

Published
2016

7. Mechanisms of hydrogen peroxide-induced vasoconstriction in the isolated perfused rat kidney

Author

Moreno, J. M., Gomez, I. R., Wangensteen, R., Perez-Abud, R., Duarte, J., Osuna, A., Vargas, F., [Moreno,JM, Rodriguez Gomez,I, Vargas,F] Departamento de Fisiología, Facultad de Medicina, Granada, Spain. [Wangensteen,R] Departamento de Ciencias de la Salud, Universidad de Jaen, Spain. [Perez-Abud,R, Osuna,A] Servicio de Nefrologia, Unidad Experimental, Hospital Virgen de las Nieves, Granada, Spain. [Duarte,J] Departamento de Farmacologia, Facultad de Farmacia, Granada, Spain., and This study was supported by a grant (CTS- 1659) Proyecto de Excelencia from Consejería de Innovación Ciencia y Empresa of the Junta de Andalucía and by the Ministerio de Sanidad y Consumo, Instituto de Salud Carlos III (Red de Investigación Renal, REDinREN D06/0016/0017 and Red HERACLES RD06/0009). Fondo Europeo de Desarrollo Regional (FEDER) 'Una manera de hacer Europa'.

Subjects
Chemicals and Drugs::Inorganic Chemicals::Free Radicals::Reactive Oxygen Species::Peroxides::Hydrogen Peroxide [Medical Subject Headings], Sexual Dimorphism, Peróxido de Hidrógeno, Anatomy::Urogenital System::Urinary Tract::Kidney [Medical Subject Headings], Hydroxyl Radical, Phenomena and Processes::Reproductive and Urinary Physiological Phenomena::Reproductive Physiological Phenomena::Sex Characteristics [Medical Subject Headings], Check Tags::Male [Medical Subject Headings], Riñón, Hydrogen Peroxide, Phenomena and Processes::Circulatory and Respiratory Physiological Phenomena::Cardiovascular Physiological Phenomena::Cardiovascular Physiological Processes::Hemodynamics::Vasoconstriction [Medical Subject Headings], Vasoconstricción, Catalase, Kidney, Radical Hidroxilo, Ca2+, Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Rats [Medical Subject Headings], Renal Perfusion Pressure, Check Tags::Female [Medical Subject Headings], Protein kinase C, Vasoconstriction, Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Oxidoreductases::Peroxidases::Catalase [Medical Subject Headings], Chemicals and Drugs::Inorganic Chemicals::Free Radicals::Reactive Oxygen Species::Hydroxyl Radical [Medical Subject Headings], Organisms::Eukaryota::Animals [Medical Subject Headings]
Abstract

Journal Article; Research Support, Non-U.S. Gov't; The vasoconstrictor effect of hydrogen peroxide (H(2)O(2)) on isolated perfused rat kidney was investigated. H(2)O(2) induced vasoconstriction in the isolated rat kidney in a concentration-dependent manner. The vasoconstrictor effects of H(2)O(2) were completely inhibited by 1200 U/ml catalase. Endothelium-removal potentiated the renal response to H(2)O(2). The H(2)O(2) dose-response curve was not significantly modified by administration of the NO inhibitor L-NAME (10(-4) mol/l), whereas it was increased by the non-specific inhibitor of K+-channels, tetraethylammonium (3.10(-3) mol/l). Separately, removal of extracellular Ca(2+), administration of a mixture of calcium desensitizing agents (nitroprusside, papaverine, and diazoxide), and administration of a protein kinase C (PKC) inhibitor (chelerythrine, 10(-5) mol/l) each significantly attenuated the vasoconstrictor response to H(2)O(2), which was virtually suppressed when they were performed together. The pressor response to H(2)O(2) was not affected by: dimethyl sulfoxide (7.10(-5) mol/l) plus mannitol (3.10(-5) mol/l); intracellular Ca(2+) chelation using BAPTA (10(-5) mol/l); calcium store depletion after repeated doses of phenylephrine (10(-5) g/g kidney); or the presence of indomethacin (10(-5) mol/l), ODYA (2.10(-6) mol/l) or genistein (10(-5) mol/l). We conclude that the vasoconstrictor response to H(2)O(2) in the rat renal vasculature comprises the following components: 1) extracellular calcium influx, 2) activation of PKC, and 3) stimulation of pathways leading to sensitization of contractile elements to calcium. Moreover, a reduced pressor responsiveness to H(2)O(2) in female kidneys was observed. Yes

Published
2010

9. Rosiglitazone, a peroxisome proliferator-activated receptor-gamma agonist, prevents microparticle-induced vascular hyporeactivity through the regulation of proinflammatory proteins

Author

Tesse, A., Al-Massarani, G., Wangensteen, R., Reitenbach, S., M Carmen Martinez, Andriantsitohaina, R., Institut Gilbert-Laustriat : Biomolécules, Biotechnologie, Innovation Thérapeutique, Université Louis Pasteur - Strasbourg I-Centre National de la Recherche Scientifique (CNRS), and Barthel, Ingrid

Subjects
[SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, [SDV.BC] Life Sciences [q-bio]/Cellular Biology
Published
2008

10. Protection against endotoxic shock as a consequence of reduced nitrosative stress in MLCK210-null mice

Author

Ralay Ranaivo, H., Carusio, N., Wangensteen, R., Ohlmann, P., Loichot, C., Tesse, A., Chalupsky, K., Lobysheva, I., Haiech, J., Watterson, D.M., Andriantsitohaina, R., Institut Gilbert-Laustriat : Biomolécules, Biotechnologie, Innovation Thérapeutique, Université Louis Pasteur - Strasbourg I-Centre National de la Recherche Scientifique (CNRS), and Barthel, Ingrid

Subjects
[SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, [SDV.BC] Life Sciences [q-bio]/Cellular Biology
Published
2007

19. Effects of Antihypertensive Drugs on Angiotensinase Activities in the Testis of Spontaneously Hypertensive Rats.

Author

Segarra, A. B., Prieto, I., Villarejo, A. B., Banegas, I., Wangensteen, R., De Gasparo, M., Vives, F., and Ramírez-Sánchez, M.

Subjects
SEXUAL dysfunction, ANTIHYPERTENSIVE agents, ANGIOTENSINS, DRUG additives, DRUG efficacy, THERAPEUTICS, DISEASE risk factors
Abstract

Sexual dysfunction is a frequent adverse effect during antihypertensive therapy. However, the mechanisms responsible for these effects are not well understood. The renin-angiotensin system has been identified in testis where it may play a role in testicular function and be involved in the detrimental effects of antihypertensive drugs. Therefore, our objective was to compare the influence of captopril and propranolol on plasma testosterone levels and on hydrolyzing angiotensin's enzymes (angiotensinases) in the testis of spontaneously hypertensive rats (SHRs) and in control animals. Twenty-four adult male SHRs were used in this study; eight were treated with captopril in drinking water, 8 with propranolol, and 8 were controls. At the end of the 4 weeks treatment period, systolic blood pressure (SBP) was recorded, blood samples were collected, and the right testis was dissected after perfusion of the rat with saline. The soluble (Sol) and membrane- bound (MB) fractions were obtained after solubilization and ultracentrifugation. Fluorometric measurement of Sol and MB angiotensinase activities were performed using arylamide derivatives as substrates. Testosterone was measured by enzyme immunoassay. SBP decreased after captopril but did not change with propranolol treatment. Whereas captopril did not affect angiotensinase activities, highly significant reductions in Sol and MB angiotensinase activities, particularly glutamyl- and aspartylaminopeptidases, were observed after treatment with propranolol. Plasma testosterone decreased in captopril treated rats but propranolol had a greater effect. The present results support a general functional depression of the RAS cascade in the testis of propranolol-treated SHR, which may influence the sexual function of these animals. [ABSTRACT FROM AUTHOR]

Published
2013
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22. Angiotensinase and Vasopressinase Activities in Hypothalamus, Plasma, and Kidney after Inhibition of Angiotensin-converting Enzyme: Basis for a New Working Hypothesis.

Author

Villarejo, A. B., Segarra, A. B., Ramírez, M., Banegas, I., Wangensteen, R., de Gasparo, M., Cobo, J., Alba, F., Vives, F., and Prieto, I.

Subjects
HYPERTENSION, ANGIOTENSIN converting enzyme, ANGIOTENSINS, VASOPRESSIN, PITUITARY hormones
Abstract

Reducing angiotensin II (Ang II) production via angiotensin-converting enzyme (ACE) inhibitors is a key approach for the treatment of hypertension. However, these inhibitors may also affect other enzymes, such as angiotensinases and vasopressinase, responsible for the metabolism of other peptides also involved in blood pressure control, such as Ang 2-10, Ang III, Ang IV, and vasopressin. We analyzed the activity of these enzymes in the hypothalamus, plasma, and kidney of normotensive adult male rats after inhibition of ACE with captopril. Aspartyl- (AspAP), glutamyl- (GluAP), alanyl- (AlaAP) and cystinyl-aminopeptidase (CysAP) activities were measured fluorimetrically using arylamides as substrates. Systolic blood pressure (SBP), water intake, and urine flow were also measured. Captopril reduced SBP and increased urine flow. In the hypothalamus, GluAP and AspAP increased, without significant changes in either AlaAP or CysAP. In contrast with effects in plasma, GluAP was unaffected, AspAP decreased, while AlaAP and CysAP increased. In the kidney, enzymatic activities did not change in the cortex, but decreased in the medulla. These data suggest that after ACE inhibition, the metabolism of Ang I in hypothalamus may lead mainly to Ang 2-10 formation. In plasma, the results suggest an increased formation of Ang IV together with increased vasopressinase activity. In the kidney, there is a reduction of vasopressinase activity in the medulla, suggesting a functional reduction of vasopressin in this location. The present data suggest the existence of alternative pathways in addition to ACE inhibition that might be involved in reducing BP after captopril treatment. [ABSTRACT FROM AUTHOR]

Published
2012
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26. Glutamyl aminopeptidase in microvesicular and exosomal fractions of urine is related with renal dysfunction in cisplatin-treated rats

Author

Manuel Gómez-Guzmán, Ana Belén Segarra, Félix Vargas, Rosemary Wangensteen, Antonio Osuna, Sebastián Montoro-Molina, María Del Carmen de Gracia, Andrés Quesada, Francisco O'Valle, [Quesada,A, de Gracia,MC, Osuna,A] Unidad de Nefrología, Hospital Virgen de las Nieves, FIBAO, Granada, Spain. [Segarra,AB, Montoro-Molina,S, Gómez-Guzmán,M, and Wangensteen,R] Área de Fisiología, Departamento de Ciencias de la Salud, Universidad de Jaén, Jaén, Spain. [O’Valle,F] Departamento de Anatomía Patológica, IBIMER, Universidad de Granada, Granada, Spain. [Vargas,F] Departamento de Fisiología, Facultad de Medicina, Universidad de Granada, Granada, Spain.

Subjects
0301 basic medicine, Male, Técnicas para inmunoenzimas, Physiology, Chemicals and Drugs::Inorganic Chemicals::Chlorine Compounds::Cisplatin [Medical Subject Headings], 030232 urology & nephrology, lcsh:Medicine, Phenomena and Processes::Physiological Phenomena::Physiological Processes::Growth and Development::Growth::Body Size::Body Weight::Body Weight Changes::Weight Gain [Medical Subject Headings], Urine, Phenomena and Processes::Physiological Phenomena::Body Constitution::Body Weights and Measures::Body Size::Body Weight [Medical Subject Headings], Exosomes, Kidney, Biochemistry, Anatomy::Cells::Cellular Structures::Extracellular Space [Medical Subject Headings], Analytical, Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Immunologic Techniques::Immunoassay::Immunoblotting [Medical Subject Headings], chemistry.chemical_compound, 0302 clinical medicine, Mathematical and Statistical Techniques, Glutamil aminopeptidasa, Organisms::Eukaryota::Animals [Medical Subject Headings], Medicine and Health Sciences, lcsh:Science, Multidisciplinary, Chemistry, Cisplatino, Diseases::Neoplasms [Medical Subject Headings], Neoplasias, Analytical, Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Immunologic Techniques::Immunoassay::Immunoenzyme Techniques [Medical Subject Headings], Body Fluids, Physiological Parameters, Creatinine, Chemicals and Drugs::Heterocyclic Compounds::Heterocyclic Compounds, 1-Ring::Azoles::Imidazoles::Creatinine [Medical Subject Headings], Physical Sciences, Regression Analysis, Creatinina, Anatomy, Cellular Structures and Organelles, Statistics (Mathematics), Research Article, medicine.medical_specialty, Aumento de peso, Excretion, Renal function, Analytical, Diagnostic and Therapeutic Techniques and Equipment::Diagnosis::Diagnostic Techniques and Procedures::Diagnostic Techniques, Urological::Kidney Function Tests [Medical Subject Headings], Linear Regression Analysis, Research and Analysis Methods, Glutamyl Aminopeptidase, Espacio extracelular, Nephrotoxicity, 03 medical and health sciences, Ratas, Internal medicine, Antígenos CD13, medicine, Animals, Vesicles, Statistical Methods, Rats, Wistar, Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Hydrolases::Peptide Hydrolases::Exopeptidases::Aminopeptidases::Antigens, CD13 [Medical Subject Headings], Analytical, Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Centrifugation [Medical Subject Headings], Differential centrifugation, lcsh:R, Body Weight, Biology and Life Sciences, Peso corporal, Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Hydrolases::Peptide Hydrolases::Exopeptidases::Aminopeptidases::Glutamyl Aminopeptidase [Medical Subject Headings], Kidneys, Cell Biology, Renal System, Rats, 030104 developmental biology, Endocrinology, Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Rats [Medical Subject Headings], Glutamyl aminopeptidase, Animales, Pruebas de función renal, Microsome, Centrifugación, lcsh:Q, Cisplatin, Physiological Processes, Biomarkers, Mathematics
Abstract

PURPOSE: The aim of this work was to investigate if the content of glutamyl aminopeptidase (GluAp) in microvesicular and exosomal fractions of urine is related with renal dysfunction in cisplatin-treated rats. METHODS: Urine samples were collected 24 hours after injection of cisplatin (7 mg/kg, n = 10) or saline serum (n = 10), and they were subjected to differential centrifugation at 1.000, 17.000 and 200.000 g to obtain microvesicular and exosomal fractions. GluAp was measured with a commercial ELISA kit in both fractions. Serum creatinine (SCr) and body weight were measured 15 days after treatment. We analyzed if early excretion of GluAp in microsomal and exosomal fractions was correlated with final SCr and body weight increase. In a second experiment, enzymatic activities of GluAp and alanyl aminopeptidase (AlaAp) in urine, microvesicular and exosomal fractions were measured three days after injection. We analyzed the correlation of both markers with SCr determined at this point. Finally, we studied the expression of GluAp and extracellular vesicles markers Alix and tumor susceptibility gene (TSG101) in both fractions by immunoblotting. RESULTS: GluAp excretion was increased in all fractions of urine after cisplatin treatment, even if data were normalized per mg of creatinine, per body weight or per total protein content of each fraction. We found significant predictive correlations with SCr concentration, and inverse correlations with body weight increase determined 15 days later. Three days after injection, aminopeptidasic activities were markedly increased in all fractions of urine in cisplatin-treated rats. The highest correlation coefficient with SCr was found for GluAp in microvesicular fraction. Increase of GluAp in microvesicular and exosomal fractions from cisplatin-treated rats was confirmed by immunoblotting. Alix and TSG101 showed different patterns of expression in each fraction. CONCLUSIONS: Determination of GluAp content or its enzymatic activity in microvesicular and exosomal fractions of urine is an early and predictive biomarker of renal dysfunction in cisplatin-induced nephrotoxicity. Measurement of GluAp in these fractions can serve to detect proximal tubular damage independently of glomerular filtration status. This study was supported by the grants PI13/02743 (AO) and PI13/02384 (RW) from the Carlos III Health Institute of Spain, and the Red de Investigación Renal REDinREN RD16/0009/0033 (AO).“FEDER una manera de hacer Europa”. Yes

Published
2017

27. Long-Term Consequences of Uninephrectomy in Male and Female Rats

Author

Francisco O'Valle, Juan de Dios Luna, Andrés Quesada, Antonio Osuna, Félix Vargas, Rocío Perez-Abud, Raimundo G. del Moral, Rosemary Wangensteen, Isabel Rodríguez-Gómez, [Rodríguez-Gómez,I, Vargas,F] Departamento de Fisiología, Facultad de Medicina, Granada, Spain. [Luna, J de D] Departamento de Bioestadística, Facultad de Medicina, Granada, Spain. [Pérez-Abud,R, Osuna,A] Servicio de Nefrología, Unidad Experimental, Hospital Virgen de las Nieves, Granada, Spain. [Wangensteen,R, Quesada,A] Departamento de Ciencias de la Salud, Universidad de Jaén, Jaén, Spain. [Moral, RG del, O’Valle, F] Departamento de Anatomía Patológica e Instituto de Biomedicina Regenerativa, Facultad de Medicina, Granada, Spain., and This study was supported by grants from the Ministry of Education and Science (SAF2009-12294), from an Excelencia project (CTS- 6704) of the Regional Government of Andalucía, and from the Carlos III Health Institute of the Spanish Ministry of Health and Consumer Affairs (Red de Investigación Renal, REDinREN RD06/0016/0017 and D07/0016/2008). FEDER una manera de hacer Europa

Subjects
medicine.medical_specialty, renal injury, Anatomy::Urogenital System::Urinary Tract::Kidney [Medical Subject Headings], Urinary system, Urology, Check Tags::Male [Medical Subject Headings], Renal function, Riñón, Biology, Health Care::Environment and Public Health::Public Health::Epidemiologic Factors::Sex Factors [Medical Subject Headings], Ratas, Basal (phylogenetics), chemistry.chemical_compound, renal sodium handling, Internal medicine, Sodio, Phenomena and Processes::Circulatory and Respiratory Physiological Phenomena::Cardiovascular Physiological Phenomena::Hemodynamics::Blood Pressure [Medical Subject Headings], Organisms::Eukaryota::Animals [Medical Subject Headings], Internal Medicine, medicine, Nefrectomía, rat, Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Rats::Rats, Wistar [Medical Subject Headings], Masculino, Phenomena and Processes::Metabolic Phenomena::Metabolism::Oxidative Stress [Medical Subject Headings], Pathological, Creatinine, Kidney, Proteinuria, Femenino, blood pressure, Presión Arterial, Ratas Wistar, Factores Sexuales, Diseases::Pathological Conditions, Signs and Symptoms::Signs and Symptoms::Urological Manifestations::Proteinuria [Medical Subject Headings], Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Rats [Medical Subject Headings], Blood pressure, Endocrinology, medicine.anatomical_structure, Uninephrectomy, Check Tags::Female [Medical Subject Headings], Analytical, Diagnostic and Therapeutic Techniques and Equipment::Surgical Procedures, Operative::Urogenital Surgical Procedures::Urologic Surgical Procedures::Nephrectomy [Medical Subject Headings], chemistry, Chemicals and Drugs::Inorganic Chemicals::Metals::Metals, Alkali::Sodium [Medical Subject Headings], medicine.symptom, Estrés Oxidativo
Abstract

We investigated the effects of uninephrectomy (UNX) in 6-week-old male and female rats on blood pressure (BP), renal sodium handling, salt sensitivity, oxidative stress, and renal injury over 18 months postsurgery, studying control sham-operated and UNX-operated rats at 6, 12, and 18 months postsurgery, evaluating their renal sodium handling, BP, urinary isoprostanes, N -acetyl-β- d -glucosaminidase, and proteinuria before and after a 2-week high-salt intake period. At 18 months, plasma variables were measured and kidney samples were taken for the analysis of renal morphology and tissue variables. BP was increased at 6 months in male UNX rats versus controls and at 12 and 18 months in both male and female UNX rats and was increased in male versus female UNX groups at 18 months. UNX did not affect water and sodium excretion under basal conditions and after the different test in male and female rats at different ages. However, the renal function curve was shifted to the right in both male and female UNX rats. High-salt intake increased BP in both UNX groups at 6, 12, and 18 months and in the female control group at 18 months, and it increased proteinuria, N -acetyl-β- d -glucosaminidase, and isoprostanes in both UNX groups throughout the study. Renal lesions at 18 months were more severe in male versus female UNX rats. In summary, long-term UNX increased the BP, creatinine, proteinuria, pathological signs of renal injury, and salt sensitivity. Earlier BP elevation was observed and morphological lesions were more severe in male than in female UNX rats.

Published
2012

28. Urinary Aminopeptidase Activities as Early and Predictive Biomarkers of Renal Dysfunction in Cisplatin-Treated Rats

Author

Sebastián Montoro-Molina, Andrés Quesada, Félix Vargas, María Dolores Rodríguez-Martínez, Manuel Ramírez, Isabel Prieto, Rosemary Wangensteen, Francisco O'Valle, Antonio Osuna, [Quesada,A, Montoro-Molina,S, Prieto,I, Ramírez,M, Wangensteen,R] Área de Fisiología, Departamento de Ciencias de la Salud, Universidad de Jaén, Jaén, Spain. [Vargas,F] Departamento de Fisiología, Facultad de Medicina, Universidad de Granada, Granada, Spain. [O'Valle,F, Rodríguez-Martínez,MD] Departamento de Anatomía Patológica, Facultad de Medicina, Universidad de Granada, IBIMER Granada, Spain. [Osuna,A] Servicio de Nefrología, Hospital Virgen de las Nieves, Granada, Spain., and This study was supported by a grant (R1/12/2010/66) from the University of Jaén with the participation of Caja Rural of Jaén, and from the Carlos III Health Institute of the Spanish Ministry of Health and Consumer Affairs (Red de Investigación Renal, REDinREN RD06/0016/0017 and RD07/0016/2008), 'FEDER una manera de hacer Europa.'

Subjects
Male, Anatomy and Physiology, Critical Care and Emergency Medicine, Chemicals and Drugs::Inorganic Chemicals::Chlorine Compounds::Cisplatin [Medical Subject Headings], lcsh:Medicine, Aminopeptidasas, Urine, Kidney, Aminopeptidases, Biochemistry, Insuficiencia Renal, chemistry.chemical_compound, Renal Critical Care, Pathology, Amino Acids, lcsh:Science, Multidisciplinary, Proteinuria, Acute kidney injury, Cisplatino, Organ Size, Animal Models, Acute Kidney Injury, Lipocalins, Enzymes, Chemistry, Organic Acids, medicine.anatomical_structure, Nephrology, Area Under Curve, Creatinine, Marcadores Biológicos, Medicine, medicine.symptom, Research Article, medicine.medical_specialty, Urinary system, Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Hydrolases::Peptide Hydrolases::Exopeptidases::Aminopeptidases [Medical Subject Headings], Excretion, Renal function, Antineoplastic Agents, Diseases::Male Urogenital Diseases::Urologic Diseases::Kidney Diseases::Renal Insufficiency [Medical Subject Headings], Model Organisms, Lipocalin-2, Diagnostic Medicine, Proto-Oncogene Proteins, Albumins, Internal medicine, Acetylglucosaminidase, Chemicals and Drugs::Biological Factors::Biological Markers [Medical Subject Headings], medicine, Albuminuria, Animals, Rats, Wistar, Biology, Enzyme Kinetics, Renal Physiology, Renal system, business.industry, Organic Chemistry, lcsh:R, Kidneys, Renal System, medicine.disease, Fibrosis, Ratas Wistar, Rats, Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Rats [Medical Subject Headings], Endocrinology, ROC Curve, chemistry, Linear Models, Rat, lcsh:Q, Cisplatin, business, Biomarkers, Acute-Phase Proteins, General Pathology
Abstract

This study analyzes the fluorimetric determination of alanyl- (Ala), glutamyl- (Glu), leucyl-cystinyl- (Cys) and aspartyl-aminopeptidase (AspAp) urinary enzymatic activities as early and predictive biomarkers of renal dysfunction in cisplatin-treated rats. Male Wistar rats (n = 8 each group) received a single subcutaneous injection of either saline or cisplatin 3.5 or 7 mg/kg, and urine samples were taken at 0, 1, 2, 3 and 14 days after treatment. In urine samples we determined Ala, Glu, Cys and AspAp activities, proteinuria, N-acetyl-β-D-glucosaminidase (NAG), albumin, and neutrophil gelatinase-associated lipocalin (NGAL). Plasma creatinine, creatinine clearance and renal morphological variables were measured at the end of the experiment. CysAp, NAG and albumin were increased 48 hours after treatment in the cisplatin 3.5 mg/kg treated group. At 24 hours, all urinary aminopeptidase activities and albuminuria were significantly increased in the cisplatin 7 mg/kg treated group. Aminopeptidase urinary activities correlated (p0.259) with plasma creatinine, creatinine clearance and/or kidney weight/body weight ratio at the end of the experiment and they could be considered as predictive biomarkers of renal injury severity. ROC-AUC analysis was made to study their sensitivity and specificity to distinguish between treated and untreated rats at day 1. All aminopeptidase activities showed an AUC>0.633. We conclude that Ala, Cys, Glu and AspAp enzymatic activities are early and predictive urinary biomarkers of the renal dysfunction induced by cisplatin. These determinations can be very useful in the prognostic and diagnostic of renal dysfunction in preclinical research and clinical practice., This study was supported by a grant (R1/12/2010/66) from the University of Jaén with the participation of Caja Rural of Jaén, and from the Carlos III Health Institute of the Spanish Ministry of Health and Consumer Affairs (Red de Investigación Renal, REDinREN RD06/0016/0017 and RD07/0016/2008), “FEDER una manera de hacer Europa.”

Published
2012

29. Aminopeptidasic Enzymes as Early Biomarkers of Cardiac Surgery-Associated Acute Kidney Injury and Long-Term Events.

Author

Rísquez Chica N, Pereira E, Manzano F, Quintana MMJ, Osuna A, Fuentes MCR, and Wangensteen R

Subjects
Humans, Male, Female, Aged, Middle Aged, Glomerular Filtration Rate, Dipeptidyl Peptidase 4 blood, Dipeptidyl Peptidase 4 urine, Dipeptidyl Peptidase 4 metabolism, Aminopeptidases urine, Aminopeptidases blood, Aminopeptidases metabolism, Creatinine blood, Creatinine urine, Lipocalin-2 urine, Lipocalin-2 blood, Acetylglucosaminidase urine, Acute Kidney Injury urine, Acute Kidney Injury diagnosis, Acute Kidney Injury blood, Acute Kidney Injury etiology, Biomarkers urine, Biomarkers blood, Cardiac Surgical Procedures adverse effects
Abstract

Background: Diagnosis of acute kidney injury (AKI) relies on serum creatinine (SCr) changes. This study investigated if urinary aminopeptidases are early and predictive biomarkers of cardiac surgery-associated AKI (CSA-AKI)., Methods: Glutamyl aminopeptidase (GluAp), alanyl aminopeptidase (AlaAp), dipeptidyl peptidase-4 (DPP4), proteinuria, albuminuria, N-acetyl-β- D -glucosaminidase (NAG), and neutrophile gelatinase-associated lipocalin (NGAL) were measured in urine samples from 44 patients at arrival in the intensive care unit (ICU) after cardiac surgery. Sensitivity, specificity, and positive and negative predictive value for diagnosis of stages 1, 2, and 3 of AKI were analyzed for the highest quartile of each marker. We also studied the relationship with SCr after surgery, 6- and 12-month glomerular filtration rates (GFRs), and other long-term events over the next 5 years., Results: GluAp diagnosed the maximal number of patients that developed stage 2 or 3 of AKI, increasing diagnostic sensitivity from 0% to 75%. In addition, GluAp and DPP4 were related to the decrease in GFR at 6 or 12 months after surgery., Conclusions: Urinary aminopeptidases are a potential tool for the early diagnosis of CSA-AKI, with GluAp being the most effective marker for diagnosing stage 2 or 3 of AKI at ICU admission. GluAp and DPP4 serve as predictive biomarkers for a decrease in GFR.

Published
2024
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30. Vasoconstrictor and Pressor Effects of Des-Aspartate-Angiotensin I in Rat.

Author

Wangensteen R, Gómez-Guzmán M, Banegas I, Rodríguez-Gómez I, Jiménez R, Duarte J, García-Estañ J, and Vargas F

Abstract

This study investigated the vasoactive effects of des-aspartate-angiotensin-I (DAA-I) in male Wistar rats on whole body vascular bed, isolated perfused kidneys, and aortic rings. Dose-response curves to DAA-I were compared with those to angiotensin II (Ang II). The Ang II-type-1 (AT1) receptor blocker, losartan, was used to evaluate the role of AT1 receptors in the responses to DAA-I. Studies were also conducted of the responsiveness in aortic rings after endothelium removal, nitric oxide synthase inhibition, or AT2 receptor blockade. DAA-I induced a dose-related systemic pressor response that was shifted to the right compared with Ang II. Losartan markedly attenuated the responsiveness to DAA-I. DAA-I showed a similar pattern in renal vasculature and aortic rings. In aortic rings, removal of endothelium and nitric oxide inhibition increased the sensitivity and maximal response to DAA-I and Ang II. AT2 receptor blockade did not significantly affect the responsiveness to DAA-I. According to these findings, DAA-I increases the systemic blood pressure and vascular tone in conductance and resistance vessels via AT1 receptor activation. This vasoconstrictor effect of DAA-I participates in the homeostatic control of arterial pressure, which can also contribute to the pathogenesis of hypertension. DAA-I may therefore be a potential therapeutic target in cardiovascular disease.

Published
2022
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31. The Long-Term Study of Urinary Biomarkers of Renal Injury in Spontaneously Hypertensive Rats.

Author

Montoro-Molina S, Quesada A, O'Valle F, Morales NM, de Gracia MDC, Rodríguez-Gómez I, Osuna A, Wangensteen R, and Vargas F

Subjects
Animals, Biomarkers urine, CD13 Antigens urine, Dipeptidyl Peptidase 4 urine, Glutamyl Aminopeptidase urine, Hypertension complications, Kidney Diseases etiology, Klotho Proteins analysis, Male, Rats, Inbred SHR, Rats, Inbred WKY, Rats, Hypertension urine, Kidney Diseases urine
Abstract

Background: The age-related increase in blood pressure in spontaneously hypertensive rats (SHRs) is associated to cardiac hypertrophy, heart failure, and renal injury. Here, we investigated for the first time the urinary enzymatic activities of glutamil aminopeptidase (GluAp), alanyl aminopeptidase (AlaAp), dipeptidyl peptidase-4 (DPP4), and Klotho urinary levels, proteins that are strongly expressed in the kidney, as early biomarkers of renal injury in SHRs., Methods: Male SHR and Wistar Kyoto (WKY) rats were studied from 2 to 8 months old. Systolic blood pressure (SBP), the heart rate (HR), metabolic variables, and urinary markers were measured monthly. At the end of the study, a histopathological evaluation of the kidney was performed., Results: Kidneys of SHR did not develop signs of relevant histopathological changes, but showed increased glomerular area and cellularity. Plasma creatinine was decreased, and creatinine clearance was augmented in SHR at the end of the study. Urinary excretion of Klotho was higher in SHR at 5 and 8 months old, whereas plasma Klotho levels were similar to WKY. GluAp, AlaAp, and DPP4 urinary activities were increased in SHR throughout the time-course study. A positive correlation between glomerular area and cellularity with creatinine clearance was observed. Urinary GluAp, AlaAp, DPP4, and Klotho showed positive correlations with SBP., Conclusions: GluAp, AlaAp, DPP4, and Klotho in the urine are useful tools for the evaluation of renal damage at early stages, before the whole histopathological and biochemical manifestations of renal disease are established. Moreover, these observations may represent a novel and noninvasive diagnostic approach to assess the evolution of kidney function in hypertension and other chronic diseases., (© 2021 The Author(s) Published by S. Karger AG, Basel.)

Published
2021
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32. Female Sexual Function and Its Association with the Severity of Menopause-Related Symptoms.

Author

Pérez-Herrezuelo I, Aibar-Almazán A, Martínez-Amat A, Fábrega-Cuadros R, Díaz-Mohedo E, Wangensteen R, and Hita-Contreras F

Subjects
Cross-Sectional Studies, Female, Humans, Postmenopause, Surveys and Questionnaires, Menopause, Sexual Dysfunction, Physiological
Abstract

The aim of this study was to examine female sexual functioning and its association with the impact of the symptoms of menopause among Spanish postmenopausal women. A total of 182 postmenopausal women (65.59 ± 7.93 years) participated in this cross-sectional study. The female sexual function index (FSFI) and the menopause rating scale (MRS) were used to analyze sexual function and severity of menopausal symptoms, respectively. Age, education, area of residence, occupation, and depression (Hospital Anxiety and Depression Scale) were considered as possible confounders. The results of a linear multivariate regression analysis showed that the severity of urogenital menopause-related symptoms was associated with lower values in the FSFI total score and the lubrication, satisfaction, arousal, and orgasm domains. These last three subscales were also linked to severe psychological impact, while the MRS total score was only related to the desire domain. Regarding confounders, being younger, working, and residing in a rural area were all linked to better sexual function. All effect sizes were large (adjusted R 2 > 0.35). In conclusion, after controlling for possible confounders, postmenopausal women who experience a severe impact of menopausal symptoms endure poorer sexual function, particularly when said symptoms are urogenital or psychological in nature.

Published
2020
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33. Effect of pulmonary vein catheter ablation on kidney function in patients with atrial fibrillation. A prospective cohort study.

Author

Macías-Ruiz R, Jiménez-Jáimez J, Álvarez-López M, Molina-Lerma M, Sánchez-Millán P, Wangensteen R, Quesada A, Osuna-Ortega A, and Tercedor-Sánchez L

Subjects
Aged, Female, Humans, Kidney surgery, Male, Middle Aged, Prospective Studies, Recurrence, Treatment Outcome, Atrial Fibrillation surgery, Catheter Ablation, Pulmonary Veins surgery
Abstract

Introduction and Objectives: Several studies have linked the presence of atrial fibrillation (AF) with reduced estimated glomerular filtration rate (eGFR). Our objective was to compare changes in eGFR in patients with AF after pulmonary vein (PV) ablation depending on the success of the technique, as well as to examine the relationship between eGFR and several biomarkers., Methods: Prospective cohort of patients with AF referred to our center for PV ablation with a 1-year follow-up. We estimated eGFR using the Chronic Kidney Disease Epidemiology Collaboration formula at baseline and at 3 and 12 months. Biomarkers (B-type natriuretic peptide, corin, and galectin-3) were measured before ablation and at 12 months., Results: We studied 124 patients (age 55±10 years, 69.4% men). Seventy-five had paroxysmal AF (60.5%). The mean baseline eGFR was 90.8 [77.8-100.0] mL/min/1.73 m 2 . The eGFR increased at the end of follow-up, with a statistically significant difference between patients with recurrence at 12 months and those without (-1.1 [-6.0 to 8.8] mL/min/1.73 m 2 vs 7.1 [-0.6 to 14.2] mL/min/1.73 m 2 , P=.017). The improvement in eGFR at 12 months was inversely proportional to baseline eGFR. B-type natriuretic peptide and corin levels improved at 12 months, while galectin-3 levels worsened, which was unrelated to eGFR., Conclusions: In patients with AF treated with PV ablation, an overall improvement in eGFR was observed, which was more marked in the subgroup without recurrences, although without significant differences on multivariate analysis., (Copyright © 2019 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.)

Published
2020
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34. The female sexual function index: reliability and validity in Spanish postmenopausal women.

Author

Pérez-Herrezuelo I, Hita-Contreras F, Martínez-Amat A, Aibar-Almazán A, Cruz-Díaz D, Wangensteen R, Ochoa AA, and Díaz-Mohedo E

Subjects
Aged, Aged, 80 and over, Factor Analysis, Statistical, Female, Humans, Middle Aged, Psychometrics, Reproducibility of Results, Spain, Visual Analog Scale, Postmenopause physiology, Postmenopause psychology, Sexual Dysfunction, Physiological diagnosis, Sexual Dysfunctions, Psychological diagnosis, Surveys and Questionnaires
Abstract

Objective: To examine the reliability and validity of the Spanish version of the Female Sexual Function Index (FSFI) and its ability to discriminate between women with and without female sexual dysfunction (FSD) among Spanish postmenopausal women., Methods: A total of 152 postmenopausal women completed the Spanish version of FSFI. Internal consistency, test-retest reliability, and construct validity (exploratory factor analysis) were analyzed. Concurrent and divergent validity were assessed using a visual analog scale for overall satisfaction with sexual life and the Hospital Anxiety and Depression Scale, respectively. To determine the ability and the accuracy of the FSFI total score in discriminating between women with and without FSD, a receiver-operating characteristic curve analysis was performed., Results: Factor analysis suggested a three-factor structure (explained variance 77.77%). The Spanish FSFI showed substantial-to-excellent test-retest reliability, with good internal consistency in the FSFI total score (Cronbach's alpha = 0.964), and also in its three dimensions. The FSFI total and domains scores showed strong (r > 0.50) and significant correlations (P < 0.01) with overall satisfaction with sexual life (concurrent validity), and low correlations with anxiety and depression (divergent validity). The Spanish FSFI total score and dimensions were significantly able to discriminate between women with and without FSD (P < 0.05), with an optimal cut-off point of <24.95 for the FSFI total score (64.15% sensitivity and 75.76% specificity)., Conclusions: The Spanish FSFI is a valid and reliable instrument for assessing and discriminating for FSD among Spanish postmenopausal women.

Published
2019
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35. Klotho and Aminopeptidases as Early Biomarkers of Renal Injury in Zucker Obese Rats.

Author

Montoro-Molina S, López-Carmona A, Quesada A, O'Valle F, Martín-Morales N, Osuna A, Vargas F, and Wangensteen R

Abstract

The aim of this study was to investigate if urinary glutamyl aminopeptidase (GluAp), alanyl aminopeptidase (AlaAp), Klotho and hydroxyproline can be considered as potential biomarkers of renal injury and fibrosis in an experimental model of obesity. Male Zucker lean (ZL) and obese (ZO) rats were studied from 2 to 8 months old. Kidneys from ZO rats at the end of the study (8 months old) developed mild focal and segmental glomerulosclerosis as well as moderate tubulointerstitial injury. Urinary excretion of Klotho was higher in ZO rats at 2, 5, and 8 months of study, plasma Klotho levels were reduced and protein abundance of Klotho in renal tissue was similar in ZL and ZO rats. GluAp and AlaAp urinary activities were also increased in ZO rats throughout the time-course study. ZO rats showed an augmentation of hydroxyproline content in renal tissue and a significant increase of tubulointerstitial fibrosis. Correlation studies demonstrated that GluAp, AlaAp, and Klotho are early diagnostic markers of renal lesions in Zucker obese rats. Proteinuria and hydroxyproline can be considered delayed diagnostic markers because their contribution to diagnosis starts later. Another relevant result is that GluAp, AlaAp, and Klotho are related not only with diagnosis but also with prognosis of renal lesions in Zucker obese rats. Moreover, strong predictive correlations of aminopeptidasic activities with the percentage of renal fibrosis or with renal hydroxyproline content at the end of the experiment were observed, indicating that an early increased excretion of these markers is related with a higher later extent of fibrosis in Zucker obese rats. In conclusion, GluAp, AlaAp, and Klotho are early diagnostic markers that are also related with the extent of renal fibrosis in Zucker obese rats. Therefore, they have a potential use not only in diagnosis, but also in prognosis of obesity-associated renal lesions.

Published
2018
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36. Thyroid hormones stimulate L-arginine transport in human endothelial cells

Author

Toral M, Jimenez R, Montoro-Molina S, Romero M, Wangensteen R, Duarte J, and Vargas F

Subjects
Calcium Signaling, Human Umbilical Vein Endothelial Cells, Humans, Integrin alphaVbeta3 metabolism, MAP Kinase Signaling System, Nitric Oxide metabolism, Nitric Oxide Synthase Type III metabolism, Amino Acid Transport Systems metabolism, Arginine metabolism, Thyroid Hormones metabolism
Abstract

Thyroid hormone activity is associated with L-arginine metabolism and nitric oxide (NO) production, which participate in the cardiovascular manifestations of thyroid disorders. L-arginine transporters play an important role in activating L-arginine uptake and NO production. However, the effects of thyroid hormones on L-arginine transporters in endothelial cells have not yet been evaluated. The following methods were used. We measured L-arginine uptake, mRNA expression of L-arginine transporters, endothelial nitric oxide synthase (eNOS) mRNA and NO generation after the administration of T3, T4 and the T3 analog, 3,3′,5-triiodothyroacetic acid TRIAC in human umbilical vein endothelial cells (HUVECs). We also analyzed the role of αvβ3 integrin and of phosphatidyl-inositol-3 kinase (PI3K), mitogen-activated protein kinases (MAPKs: ERK1/2, p38 and SAPK-JNK) and intracellular calcium signaling pathways as underlying mechanisms. To this end, αvβ3 integrin was pharmacologically inhibited by tetraiodothyroacetic acid (TETRAC) or genetically blocked by silencing αv mRNA and PI3K, MAPKs and intracellular calcium by selective inhibitors. The following results were obtained. Thyroid hormones and the T3 analog TRIAC increased L-arginine uptake in HUVECs, the sodium-independent y+/CAT isoforms, except CAT2b, sodium-dependent y+L system and sodium-independent system b0,+L-arginine transporters, eNOS mRNA and NO production. These effects were suppressed by αvβ3 integrin inhibition with TETRAC or αv integrin downregulation or by PI3K, MAPK or intracellular Ca2+ signaling inhibitors. In conclusion, we report for the first time that activation of L-arginine uptake by thyroid hormones is related to an upregulation of L-arginine transporters. This effect seems to be mediated by activation of αvβ3 integrin receptor and subsequent PI3K, MAPK and intracellular Ca2+ signaling pathways., (2018 Society for Endocrinology)

Published
2018
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37. 5-aminoisoquinoline improves renal function and fibrosis during recovery phase of cisplatin-induced acute kidney injury in rats.

Author

Quesada A, O'Valle F, Montoro-Molina S, Gómez-Morales M, Caba-Molina M, González JF, de Gracia MC, Osuna A, Vargas F, and Wangensteen R

Subjects
Animals, Cisplatin pharmacology, Fibrosis, Kidney Function Tests, Male, Rats, Rats, Wistar, Acute Kidney Injury chemically induced, Acute Kidney Injury drug therapy, Acute Kidney Injury metabolism, Cisplatin adverse effects, Isoquinolines pharmacology, Kidney metabolism, Kidney pathology
Abstract

The aim of the present study is to analyze the effects of 5-aminoisoquinoline (5-AIQ), a poly(ADP-ribose) polymerase-1 (PARP1) inhibitor, over renal dysfunction and fibrosis during recovery phase of cisplatin (CisPt)-induced acute kidney injury (AKI) in rats. Male Wistar rats were distributed in three groups ( n =8 each group): control, CisPt, and CisPt + 5-AIQ. Control and CisPt groups received a subcutaneous injection of either saline or 7 mg/kg CisPt, respectively. CisPt + 5-AIQ group received two intraperitoneal injections of 10 mg/kg 5-AIQ 2 h before and 24 h after CisPt treatment. Thirteen days after the treatment, rats were housed in metabolic cages and 24-h urine collection was made. At day 14, CisPt-treated rats showed increased diuresis, N-acetyl-β-d-glucosaminidase (NAG) excretion, glucosuria and sodium fractional excretion (NaFE), and decreased creatinine clearance (CrCl). 5-AIQ significantly increased CrCl and decreased NAG excretion, glucosuria, and NaFE. In plasma, CisPt increased sodium, urea, and creatinine concentrations, while 5-AIQ treatment decreased these variables to the levels of control group. 5-AIQ completely prevented the body weight loss evoked by CisPt treatment. CisPt also induced an increased renal expression of PAR polymer, α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1), and collagen-IV. These variables were decreased in CisPt + 5-AIQ group. Tubular lesions and renal fibrosis were also decreased by 5-AIQ treatment. We conclude that inhibition of PARP1 with 5-AIQ can attenuate long-term nephrotoxic effects associated with the CisPt treatment, preventing renal dysfunction and body weight decrease and ameliorating tubular lesions and collagen deposition., (© 2018 The Author(s).)

Published
2018
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38. Hyperthyroidism, but not hypertension, impairs PITX2 expression leading to Wnt-microRNA-ion channel remodeling.

Author

Lozano-Velasco E, Wangensteen R, Quesada A, Garcia-Padilla C, Osorio JA, Ruiz-Torres MD, Aranega A, and Franco D

Subjects
Animals, Mice, Mice, Mutant Strains, Rats, Rats, Wistar, Reactive Oxygen Species metabolism, Homeobox Protein PITX2, Homeodomain Proteins genetics, Hypertension genetics, Hyperthyroidism genetics, Ion Channels metabolism, MicroRNAs metabolism, Transcription Factors genetics, Wnt Proteins metabolism
Abstract

PITX2 is a homeobox transcription factor involved in embryonic left/right signaling and more recently has been associated to cardiac arrhythmias. Genome wide association studies have pinpointed PITX2 as a major player underlying atrial fibrillation (AF). We have previously described that PITX2 expression is impaired in AF patients. Furthermore, distinct studies demonstrate that Pitx2 insufficiency leads to complex gene regulatory network remodeling, i.e. Wnt>microRNAs, leading to ion channel impairment and thus to arrhythmogenic events in mice. Whereas large body of evidences has been provided in recent years on PITX2 downstream signaling pathways, scarce information is available on upstream pathways influencing PITX2 in the context of AF. Multiple risk factors are associated to the onset of AF, such as e.g. hypertension (HTN), hyperthyroidism (HTD) and redox homeostasis impairment. In this study we have analyzed whether HTN, HTD and/or redox homeostasis impact on PITX2 and its downstream signaling pathways. Using rat models for spontaneous HTN (SHR) and experimentally-induced HTD we have observed that both cardiovascular risk factors lead to severe Pitx2 downregulation. Interesting HTD, but not SHR, leads to up-regulation of Wnt signaling as well as deregulation of multiple microRNAs and ion channels as previously described in Pitx2 insufficiency models. In addition, redox signaling is impaired in HTD but not SHR, in line with similar findings in atrial-specific Pitx2 deficient mice. In vitro cell culture analyses using gain- and loss-of-function strategies demonstrate that Pitx2, Zfhx3 and Wnt signaling influence redox homeostasis in cardiomyocytes. Thus, redox homeostasis seems to play a pivotal role in this setting, providing a regulatory feedback loop. Overall these data demonstrate that HTD, but not HTN, can impair Pitx2>>Wnt pathway providing thus a molecular link to AF.

Published
2017
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39. Glutamyl aminopeptidase in microvesicular and exosomal fractions of urine is related with renal dysfunction in cisplatin-treated rats.

Author

Quesada A, Segarra AB, Montoro-Molina S, de Gracia MD, Osuna A, O'Valle F, Gómez-Guzmán M, Vargas F, and Wangensteen R

Subjects
Animals, Cisplatin toxicity, Kidney enzymology, Kidney physiopathology, Male, Rats, Rats, Wistar, Cisplatin administration & dosage, Exosomes enzymology, Glutamyl Aminopeptidase urine, Kidney drug effects
Abstract

Purpose: The aim of this work was to investigate if the content of glutamyl aminopeptidase (GluAp) in microvesicular and exosomal fractions of urine is related with renal dysfunction in cisplatin-treated rats., Methods: Urine samples were collected 24 hours after injection of cisplatin (7 mg/kg, n = 10) or saline serum (n = 10), and they were subjected to differential centrifugation at 1.000, 17.000 and 200.000 g to obtain microvesicular and exosomal fractions. GluAp was measured with a commercial ELISA kit in both fractions. Serum creatinine (SCr) and body weight were measured 15 days after treatment. We analyzed if early excretion of GluAp in microsomal and exosomal fractions was correlated with final SCr and body weight increase. In a second experiment, enzymatic activities of GluAp and alanyl aminopeptidase (AlaAp) in urine, microvesicular and exosomal fractions were measured three days after injection. We analyzed the correlation of both markers with SCr determined at this point. Finally, we studied the expression of GluAp and extracellular vesicles markers Alix and tumor susceptibility gene (TSG101) in both fractions by immunoblotting., Results: GluAp excretion was increased in all fractions of urine after cisplatin treatment, even if data were normalized per mg of creatinine, per body weight or per total protein content of each fraction. We found significant predictive correlations with SCr concentration, and inverse correlations with body weight increase determined 15 days later. Three days after injection, aminopeptidasic activities were markedly increased in all fractions of urine in cisplatin-treated rats. The highest correlation coefficient with SCr was found for GluAp in microvesicular fraction. Increase of GluAp in microvesicular and exosomal fractions from cisplatin-treated rats was confirmed by immunoblotting. Alix and TSG101 showed different patterns of expression in each fraction., Conclusions: Determination of GluAp content or its enzymatic activity in microvesicular and exosomal fractions of urine is an early and predictive biomarker of renal dysfunction in cisplatin-induced nephrotoxicity. Measurement of GluAp in these fractions can serve to detect proximal tubular damage independently of glomerular filtration status.

Published
2017
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40. L-Arginine metabolism in cardiovascular and renal tissue from hyper- and hypothyroid rats.

Author

Rodríguez-Gómez I, Moliz JN, Quesada A, Montoro-Molina S, Vargas-Tendero P, Osuna A, Wangensteen R, and Vargas F

Subjects
Animals, Aorta metabolism, Liver metabolism, Male, Metabolic Networks and Pathways drug effects, Rats, Wistar, Arginine metabolism, Hyperthyroidism pathology, Hypothyroidism pathology, Kidney metabolism, Myocardium metabolism, Thyroid Hormones metabolism
Abstract

This study assessed the effects of thyroid hormones on the enzymes involved in l-arginine metabolism and the metabolites generated by the different metabolic pathways. Compounds of l-arginine metabolism were measured in the kidney, heart, aorta, and liver of euthyroid, hyperthyroid, and hypothyroid rats after 6 weeks of treatment. Enzymes studied were NOS isoforms (neuronal [nNOS], inducible [iNOS], and endothelial [eNOS]), arginases I and II, ornithine decarboxylase (ODC), ornithine aminotransferase (OAT), and l-arginine decarboxylase (ADC). Metabolites studied were l-arginine, l-citrulline, spermidine, spermine, and l-proline. Kidney heart and aorta levels of eNOS and iNOS were augmented and reduced (P < 0.05, for each tissue and enzyme) in hyper- and hypothyroid rats, respectively. Arginase I abundance in aorta, heart, and kidney was increased (P < 0.05, for each tissue) in hyperthyroid rats and was decreased in kidney and aorta of hypothyroid rats (P < 0.05, for each tissue). Arginase II was augmented in aorta and kidney (P < 0.05, for each tissue) of hyperthyroid rats and remained unchanged in all organs of hypothyroid rats. The substrate for these enzymes, l-arginine, was reduced (P < 0.05, for all tissues) in hyperthyroid rats. Levels of ODC and spermidine, its product, were increased and decreased (P < 0.05) in hyper- and hypothyroid rats, respectively, in all organs studied. OAT and proline levels were positively modulated by thyroid hormones in liver but not in the other tissues. ADC protein levels were positively modulated by thyroid hormones in all tissues. According to these findings, thyroid hormone treatment positively modulates different l-arginine metabolic pathways. The changes recorded in the abundance of eNOS, arginases I and II, and ADC protein in renal and cardiovascular tissues may play a role in the hemodynamic and renal manifestations observed in thyroid disorders. Furthermore, the changes in ODC and spermidine might contribute to the changes in cardiac and renal mass observed in thyroid disorders., (© 2015 by the Society for Experimental Biology and Medicine.)

Published
2016
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41. Effects of Arginase Inhibition in Hypertensive Hyperthyroid Rats.

Author

Rodríguez-Gómez I, Manuel Moreno J, Jimenez R, Quesada A, Montoro-Molina S, Vargas-Tendero P, Wangensteen R, and Vargas F

Subjects
Animals, Arginase metabolism, Arginine pharmacology, Arginine therapeutic use, Blood Pressure, Brain Stem metabolism, Drug Evaluation, Preclinical, Heart Rate, Hypertension etiology, Hypertension metabolism, Hyperthyroidism complications, Hyperthyroidism metabolism, Isoprostanes urine, Male, Nitric Oxide blood, Random Allocation, Rats, Wistar, Renal Circulation drug effects, Thyroid Hormones blood, Arginase antagonists & inhibitors, Arginine analogs & derivatives, Hypertension drug therapy, Hyperthyroidism drug therapy
Abstract

Background: This study analyzed the effects of chronic administration of N[omega]-hydroxy-nor-l-arginine (nor-NOHA), an inhibitor of arginase, on the hemodynamic, oxidative stress, morphologic, metabolic, and renal manifestations of hyperthyroidism in rats., Methods: Four groups of male Wistar rats were used: control, nor-NOHA-treated (10 mg/kg/day), thyroxine (T4)-treated (75 μg/rat/day), and thyroxine- plus nor-NOHA-treated rats. All treatments were maintained for 4 weeks. Body weight, tail systolic blood pressure (SBP), and heart rate (HR) were recorded weekly. Finally, morphologic, metabolic, plasma, and renal variables were measured. Arginase I and II protein abundance and arginase activity were measured in aorta, heart, and kidney., Results: The T4 group showed increased arginase I and II protein abundance, arginase activity, SBP, HR, plasma nitrates/nitrites (NOx), brainstem and urinary isoprostanes, proteinuria and cardiac and renal hypertrophy in comparison to control rats. In hyperthyroid rats, chronic nor-NOHA prevented the increase in SBP and HR and decreased proteinuria in association with an increase in plasma NOx and a decrease in brainstem and urinary isoprostanes. In normal rats, nor-NOHA treatment did not significantly change any hemodynamic, morphologic, or renal variables. Acute nor-NOHA administration did not affect renal or systemic hemodynamic variables in normal or T4-treated rats., Conclusion: Hyperthyroidism in rats is associated with the increased expression and activity of arginase in aorta, heart, and kidney. Chronic arginase inhibition with nor-NOHA suppresses the characteristic hemodynamic manifestations of hyperthyroidism in association with a reduced oxidative stress. These results indicate an important role for arginase pathway alterations in the cardiovascular and renal abnormalities of hyperthyroidism., (© American Journal of Hypertension, Ltd 2015. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Published
2015
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42. Tissue distribution of CysAP activity and its relationship to blood pressure and water balance.

Author

Prieto I, Villarejo AB, Segarra AB, Wangensteen R, Banegas I, de Gasparo M, Vanderheyden P, Zorad S, Vives F, and Ramírez-Sánchez M

Subjects
Animals, Antihypertensive Agents pharmacology, Blood Pressure drug effects, Captopril pharmacology, Male, Organ Specificity drug effects, Rats, Rats, Inbred SHR, Rats, Inbred WKY, Water-Electrolyte Balance drug effects, Blood Pressure physiology, Cystinyl Aminopeptidase metabolism, Hippocampus enzymology, Kidney Medulla enzymology, Water-Electrolyte Balance physiology
Abstract

Aims: To better understand the functional role of soluble (Sol) and membrane-bound (MB) cystinyl-aminopeptidase (CysAP) activities, we studied differentially their organ distribution in adult male Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR)with or without treatment with captopril.We searched for a possible tissue-specific association of CysAP with water balance and blood pressure., Main Methods: We used twenty WKY rats distributed in ten controls and ten captopril-treated, and sixteen SHR divided in eight controls and eight captopril-treated. Captopril (100 mg/kg/day) was administered in drinking water for 4 weeks. Systolic blood pressure, water intake and diuresis were measured individually. CysAP was assayed fluorometrically using L-cystine-di-β-naphthylamide as substrate., Key Findings: Sol or MB activities were generally higher in SHR compared to WKY notably in hypothalamus and kidney than in the other tissues. Captopril mainly decreased CysAP in SHR whereas it increased in WKY. The distribution of Sol CysAP was more homogeneous among tissues ofWKY than SHR. In contrast, the distribution of MB CysAP was more heterogeneous than Sol CysAP in both WKY and SHR. This suggests that MB CysAP activity acts in a more tissue-specific manner than Sol CysAP. The majority of the significant correlations between tissue activities and the measured physiological parameters were observed mostly in renal medulla and hypothalamus., Significance: Sol and MB CysAP activities, acting separately or in concert and mainly in renal medulla, regulate the function of their susceptible endogenous substrates, and may participate meaningfully in the control of blood pressure and fluid balance.

Published
2015
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43. Immunological detection of glutamyl aminopeptidase in urine samples from cisplatin-treated rats.

Author

Montoro-Molina S, Quesada A, Zafra-Ruiz PV, O'Valle F, Vargas F, de Gracia Mdel C, Osuna A, and Wangensteen R

Subjects
Animals, Blotting, Western, Male, ROC Curve, Rats, Wistar, Renal Insufficiency chemically induced, Renal Insufficiency enzymology, Renal Insufficiency urine, Antineoplastic Agents toxicity, Cisplatin toxicity, Glutamyl Aminopeptidase urine
Abstract

Purpose: The aim of this work is to demonstrate if urinary excretion of glutamyl aminopeptidase (GluAp) can be quantified by immunological methods., Experimental Design: Urine samples from control and cisplatin-treated rats (n = 10 each group) were obtained at 1, 8, and 15 days after cisplatin injection. GluAp was analyzed by kinetic fluorimetry, ELISA, and immunoblotting. Sensitivity and specificity was studied for fluorimetric activity and ELISA 24 h after cisplatin injection. We also analyzed the predictive value over renal dysfunction at the end of the experiment., Results: GluAp was easily detected by immunoblotting and ELISA, and its urinary excretion was increased in cisplatin-treated rats (p < 0.01). Results obtained with ELISA were strongly correlated (r = 0.8186; p < 0.0001) with fluorimetric activity. Kinetic fluorimetry was the method with the highest AUC (AUC = 1) and the highest predictive value over serum creatinine (r = 0.7630; p = 0.0001) and body weight increase (r = -0.8721; p < 0.0001)., Conclusions and Clinical Relevance: GluAp can be detected in urine samples with immunological methods, making possible the development of an antibody-based kit for its determination. Its excretion correlates with the extent of renal dysfunction in cisplatin-treated rats, confirming its value as an early marker of renal damage that can be a diagnostic aid in renal diseases., (© 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Published
2015
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44. Interaction of neuropeptidase activities in cortico-limbic regions after acute restraint stress.

Author

Hernández J, Prieto I, Segarra AB, de Gasparo M, Wangensteen R, Villarejo AB, Banegas I, Vives F, Cobo J, and Ramírez-Sánchez M

Subjects
Aminopeptidases analysis, Animals, Anti-Anxiety Agents metabolism, Enkephalins metabolism, Male, Neural Pathways enzymology, Oxytocin metabolism, Rats, Rats, Wistar, Restraint, Physical, Vasopressins metabolism, Aminopeptidases metabolism, Amygdala enzymology, Hippocampus enzymology, Prefrontal Cortex enzymology, Stress, Psychological enzymology
Abstract

Brain enkephalin, vasopressin and oxytocin are anxiolytic agents involved in the stress response. Acute restraint stress influences certain neuropeptidase activities, such as some enkephalin-degrading peptidases and vasopressinase/oxytocinase, in the medial prefrontal cortex (mPFC), amygdala (AM) or hippocampus (HC), which are involved in this response. Because these regions form a unified circuit and cooperate in their response to stress, it is important to analyze the profile of the regional distribution of these activities as well as their inter-regional model of interaction in this circuit. Regarding the regional study, although most activities showed a marked predominance of the AM over the HC and mPFC, both in control and stressed animals, enkephalin-degrading activity, assayed as membrane-bound alanyl aminopeptidase activity, showed a change after stress, increasing in the HC and decreasing in the AM. The correlational study in controls indicated essentially a positive interaction between the mPFC and AM. In marked contrast, there was a highly significant change in the functional status of this circuit after stress, showing mainly a positive correlation between the mPFC and HC and between the AM and HC. The existence of correlations does not demonstrate a direct relationship between regions. However, reasons for such strong associations after restraint stress should be examined. The present study may indicate a connection between neuropeptidase activities and their corresponding neuropeptidergic substrates due to significant changes in the functional status of the cortico-limbic circuit after restraint stress., (Copyright © 2015 The Authors. Published by Elsevier B.V. All rights reserved.)

Published
2015
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45. Dietary salt restriction in hyperthyroid rats. Differential influence on left and right ventricular mass.

Author

Wangensteen R, Rodríguez-Gómez I, Perez-Abud R, Quesada A, Montoro-Molina S, Osuna A, and Vargas F

Subjects
Animals, Blood Pressure, Disease Models, Animal, Heart Rate, Kidney Function Tests, Male, Rats, Wistar, Diet methods, Hyperthyroidism pathology, Hyperthyroidism therapy, Myocardium pathology, Salts administration & dosage
Abstract

This study assessed the impact of salt restriction on cardiac morphology and biochemistry and its effects on hemodynamic and renal variables in experimental hyperthyroidism. Four groups of male Wistar rats were used: control, hyperthyroid, and the same groups under low salt intake. Body weight, blood pressure (BP), and heart rate (HR) were recorded weekly for 4 weeks. Morphologic, metabolic, plasma, cardiac, and renal variables were also measured. Low salt intake decreased BP in T(4)-treated rats but not in controls. Low salt intake reduced relative left ventricular mass but increased absolute right ventricular weight and right ventricular weight/BW ratio in both control and hyperthyroid groups. Low salt intake increased Na(+)/H(+) exchanger-1 (NHE-1) protein abundance in both ventricles in normal rats but not in hyperthyroid rats, independently of its effect on ventricular mass. Mammalian target of rapamycin (mTOR) protein abundance was not related to left or right ventricular mass in hyperthyroid or controls rats under normal or low salt conditions. Proteinuria was increased in hyperthyroid rats and attenuated by low salt intake. In this study, low salt intake produced an increase in right ventricular mass in normal and hyperthyroid rats. Changes in the left or right ventricular mass of control and hyperthyroid rats under low salt intake were not explained by the NHE-1 or mTOR protein abundance values observed. In hyperthyroid rats, low salt intake also slightly reduced BP and decreased HR, proteinuria, and water and sodium balances., (© 2014 by the Society for Experimental Biology and Medicine.)

Published
2015
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46. The pro-oxidant buthionine sulfoximine (BSO) reduces tumor growth of implanted Lewis lung carcinoma in mice associated with increased protein carbonyl, tubulin abundance, and aminopeptidase activity.

Author

Rodríguez-Gómez I, Carmona-Cortés J, Wangensteen R, Vargas-Tendero P, Banegas I, Quesada A, García-Lora AM, and Vargas F

Subjects
Animals, Carcinoma, Lewis Lung metabolism, Carcinoma, Lewis Lung pathology, Cells, Cultured, Male, Mice, Mice, Inbred CBA, Oxidative Stress, Thyroxine analogs & derivatives, Thyroxine pharmacology, Aminopeptidases metabolism, Buthionine Sulfoximine pharmacology, Carcinoma, Lewis Lung drug therapy, Protein Carbonylation, Tubulin metabolism
Abstract

This study evaluated the effects of the pro-oxidant buthionine sulfoximine (BSO) and of the interaction between BSO and TETRAC, an antagonist of αvß3 integrin, on tumor development and aminopeptidase (AP) activity in a murine model of implanted Lewis's carcinoma. Male CBA-C57 mice were untreated (controls) or treated with BSO (222 mg/100 mL in drinking water), TETRAC (10 mg/kg/day, i.p.), or BSO + TETRAC. BSO for 28 days and TETRAC were given for the last 20 days. Mice were subcutaneously inoculated with 1 × 10(6) Lewis carcinoma 3LL cells into the dorsum. Study variables were tumor weight (TW); Hb, as index of tumor-mediated angiogenesis; vascular endothelial growth factor (VEGF) protein abundance; protein carbonyl content; α-tubulin abundance; and GluAp, AlaAp, and AspAp activities. BSO produced a major decrease in TW (203 ± 18 mg) with respect to controls (365 ± 26) and a reduction in Hb content. The TETRAC group also showed marked reductions in TW (129 ± 15) and Hb concentration associated with a reduced VEGF content. The BSO + TETRAC group showed a major TW reduction (125 ± 13); although, the difference with the TETRAC group was not significant. BSO treatment increased protein carbonyl and tubulin abundance in comparison to controls. The activity of all APs was increased in the three experimental groups and was strongly and negatively correlated with TW. In conclusion, administration of BSO reduced the TW, which inversely correlated with protein carbonyl content, suggesting a loss of microtubule polymerization. The finding of a negative correlation between TW and AP activity opens up new perspectives for the study of APs as tumor growth modulators.

Published
2014
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47. Effect of thyroid hormone-nitric oxide interaction on tumor growth, angiogenesis, and aminopeptidase activity in mice.

Author

Carmona-Cortés J, Rodríguez-Gómez I, Wangensteen R, Banegas I, García-Lora ÁM, Quesada A, Osuna A, and Vargas F

Subjects
Animals, Carcinoma, Lewis Lung blood supply, Carcinoma, Lewis Lung enzymology, Cell Proliferation, Guanidines pharmacology, Hemoglobins analysis, Male, Mice, Mice, Inbred CBA, NG-Nitroarginine Methyl Ester pharmacology, Nitric Oxide Synthase Type II analysis, Thyroxine analogs & derivatives, Thyroxine pharmacology, Aminopeptidases metabolism, Carcinoma, Lewis Lung pathology, Nitric Oxide physiology, Thyroid Hormones physiology
Abstract

This study evaluated the effects of thyroid hormone-NO interaction on tumor development, vascularization, vascular endothelial growth factor (VEGF), and aminopeptidase (AP) activity in a murine model of implanted Lewis's carcinoma. Experiments were performed in male CBA-C57 mice. Animals were untreated (controls) or treated with: T4, the antithyroid drug methimazole, the NO inhibitor L-NAME, T4+L-NAME, methimazole+NAME, the αvß3 integrin antagonist tetrac, T4+tetrac, the iNOS inhibitor aminoguanidine (AG), and T4 + AG; all treatments were for 6 weeks except for tetrac, administered for the last 11 days. Mice were subcutaneously inoculated with 1 × 10(6) exponentially growing Lewis carcinoma 3LL cells into the dorsum. Study variables 9 days later were tumor weight (TW), Hb content, an index of tumor vascularization, VEGF, and AP activity. T4 produced parallel increases in TW and angiogenesis. L-NAME reduced TW and angiogenesis in control, hyperthyroid, and hypothyroid mice, whereas AG had no effect on these variables. Tetrac arrested TW in normal and T4-treated mice but did not decrease angiogenesis in T4-treated animals. Negative correlations were found between TW and AP activity in tumors from control hyper- and hypothyroid groups and an inverse relationship was observed between TW and AP activities in tetrac-treated mice. T4 enhances TW and angiogenesis, in which NO participates, but requires activation of integrin αvß3 to promote carcinogenesis. NO blockade reduces TW, regardless of the thyroid status. Thyroid hormone negatively modulates AP activity in the tumor. Accordingly, blockade of the membrane TH receptor αvß3 integrin reduces TW associated with an increase in AP activity.

Published
2014
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48. Brain, heart and kidney correlate for the control of blood pressure and water balance: role of angiotensinases.

Author

Prieto I, Villarejo AB, Segarra AB, Banegas I, Wangensteen R, Martinez-Cañamero M, de Gasparo M, Vives F, and Ramírez-Sánchez M

Subjects
Animals, Antihypertensive Agents pharmacology, Enzyme Inhibitors pharmacology, Heart Ventricles drug effects, Hypothalamus drug effects, Kidney drug effects, Male, NG-Nitroarginine Methyl Ester pharmacology, Nitric Oxide metabolism, Propranolol pharmacology, Rats, Inbred SHR, Rats, Inbred WKY, Blood Pressure physiology, Endopeptidases metabolism, Heart Ventricles enzymology, Hypothalamus enzymology, Kidney enzymology, Water-Electrolyte Balance physiology
Abstract

The renin-angiotensin system (RAS) plays a major role in the control of blood pressure (BP) and water balance by coordinating brain, heart and kidney functions, connected with each other by hormonal and neural mechanisms through the autonomic nervous system (ANS). RAS function may be monitored by the study of the enzymes (angiotensinases) involved in the metabolism of its active peptides. In order to study the relationship between the brain-heart-kidney axis and the control of BP and water balance, we analyzed the correlation of angiotensinase activities, assayed as arylamidase activities, between hypothalamus, left ventricle, renal cortex and renal medulla, collected from Wistar-Kyoto and spontaneously hypertensive rats, treated or not treated with L-NAME [N(G)-nitro-L-arginine methyl ester]. This compound not only inhibits the formation of nitric oxide but also disrupts the normal function of the ANS activating the sympathetic nervous system (SNS) to increase BP. In addition, to assess the influence of the SNS, we studied the effect of its blockade by treatment of both strains with propranolol. The present results support the notion that RAS function of the brain-heart-kidney axis, as reflected by the activities of angiotensinases, is reciprocally connected by afferent and efferent mechanisms between these locations, presumably through the ANS. These results reveal new aspects of neuroendocrine regulation possibly involving the ANS., (© 2015 S. Karger AG, Basel.)

Published
2014
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49. Influence of thyroid state on cardiac and renal capillary density and glomerular morphology in rats.

Author

Rodríguez-Gómez I, Banegas I, Wangensteen R, Quesada A, Jiménez R, Gómez-Morales M, O'Valle F, Duarte J, and Vargas F

Subjects
Animals, Coronary Vessels metabolism, Fibroblast Growth Factor 2 blood, Fibroblast Growth Factor 2 metabolism, Glomerular Mesangium blood supply, Glomerular Mesangium metabolism, Glomerular Mesangium pathology, Heart Ventricles metabolism, Heart Ventricles pathology, Hyperthyroidism blood, Hyperthyroidism metabolism, Hyperthyroidism physiopathology, Hypothyroidism blood, Hypothyroidism metabolism, Hypothyroidism physiopathology, Hypoxia-Inducible Factor 1, alpha Subunit blood, Hypoxia-Inducible Factor 1, alpha Subunit metabolism, Kidney metabolism, Kidney pathology, Kidney physiopathology, Kidney Glomerulus blood supply, Kidney Glomerulus metabolism, Kidney Glomerulus physiopathology, Male, Microvessels metabolism, Platelet Endothelial Cell Adhesion Molecule-1 metabolism, Podocytes metabolism, Podocytes pathology, Proteinuria etiology, Rats, Rats, Wistar, Ribonuclease, Pancreatic blood, Ribonuclease, Pancreatic metabolism, Thyroid Hormones blood, Thyroid Hormones metabolism, Vascular Endothelial Growth Factor A blood, Vascular Endothelial Growth Factor A metabolism, Coronary Vessels pathology, Hyperthyroidism pathology, Hypothyroidism pathology, Kidney blood supply, Kidney Glomerulus pathology, Microvessels pathology
Abstract

The purpose was to analyse the cardiac and renal capillary density and glomerular morphology resulting from a chronic excess or deficiency of thyroid hormones (THs) in rats. We performed histopathological, morphometrical and immunohistochemical analyses in hypothyroid and hyperthyroid rats to evaluate the density of mesenteric, renal and cardiac vessels at 4 weeks after induction of thyroid disorders. The main angiogenic factors in plasma, heart and kidney were measured as possible mediators of vascular changes. Mesenteric vessel branching was augmented and decreased in hyper- and hypothyroid rats respectively. The numerical density of CD31-positive capillaries was higher in left and right ventricles and in cortical and medullary kidney from both hyper- and hypothyroid rats vs controls. Numbers of podocytes and glomeruli per square millimetre were similar among groups. Glomerular area and percentage mesangium were greater in the hyperthyroid vs control or hypothyroid groups. No morphological renal lesions were observed in any group. Vascularisation of the mesenteric bed is related to TH levels, but an increased capillarity was observed in heart and kidney in both thyroid disorders. This increase may be produced by higher tissue levels of angiogenic factors in hypothyroid rats, whereas haemodynamic factors would predominate in hyperthyroid rats. Our results also indicate that the renal dysfunctions of thyroid disorders are not related to cortical or medullary microvascular rarefaction and that the proteinuria of hyperthyroidism is not secondary to a podocyte deficit. Finally, TH or its analogues may be useful to increase capillarity in renal diseases associated with microvascular rarefaction.

Published
2013
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50. The brain-heart connection: frontal cortex and left ventricle angiotensinase activities in control and captopril-treated hypertensive rats-a bilateral study.

Author

Segarra AB, Prieto I, Banegas I, Villarejo AB, Wangensteen R, de Gasparo M, Vives F, and Ramírez-Sánchez M

Abstract

The model of neurovisceral integration suggests that the frontal cortex (FC) and the cardiovascular function are reciprocally and asymmetrically connected. We analyzed several angiotensinase activities in the heart left ventricle (VT) of control and captopril-treated SHR, and we search for a relationship between these activities and those determined in the left and right FC. Captopril was administered in drinking water for 4 weeks. Samples from the left VT and from the left and right FC were obtained. Soluble and membrane-bound enzymatic activities were measured fluorometrically using arylamides as substrates. The weight of heart significantly decreased after treatment with captopril, mainly, due to the reduction of the left VT weight. In the VT, no differences for soluble activities were observed between control and treated SHR. In contrast, a generalized significant reduction was observed for membrane-bound activities. The most significant correlations between FC and VT were observed in the right FC of the captopril-treated group. The other correlations, right FC versus VT and left FC versus VT in controls and left FC versus VT in the captopril group, were few and low. These results confirm that the connection between FC and cardiovascular system is asymmetrically organized.

Published
2013
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