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299 results on '"Kuppe, Hermann"'

2. Role of Transient Receptor Potential Vanilloid 4 in Neutrophil Activation and Acute Lung Injury

Author

Yin, Jun, Michalick, Laura, Tang, Christine, Tabuchi, Arata, Goldenberg, Neil, Dan, Qinghong, Awwad, Khader, Wang, Liming, Erfinanda, Lasti, Nouailles, Geraldine, Witzenrath, Martin, Vogelzang, Alexis, Lv, Lu, Lee, Warren L., Zhang, Haibo, Rotstein, Ori, Kapus, Andras, Szaszi, Katalin, Fleming, Ingrid, Liedtke, Wolfgang B., Kuppe, Hermann, and Kuebler, Wolfgang M.

Published
2016
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4. Urinary Neutrophil Gelatinase–Associated Lipocalin/Hepcidin-25 Ratio for Early Identification of Patients at Risk for Renal Replacement Therapy After Cardiac Surgery: A Substudy of the BICARBONATE Trial

Author

Elitok, Saban, primary, Kuppe, Hermann, additional, Devarajan, Prasad, additional, Bellomo, Rinaldo, additional, Isermann, Berend, additional, Westphal, Sabine, additional, Kube, Johanna, additional, Albert, Christian, additional, Ernst, Martin, additional, Kropf, Siegfried, additional, Haase-Fielitz, Anja, additional, and Haase, Michael, additional

Published
2021
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10. Hypoxic pulmonary vasoconstriction requires connexin 40-mediated endothelial signal conduction

Author

Wang, Liming, Yin, Jun, Nickles, Hannah T., Ranke, Hannes, Tabuchi, Arata, Hoffmann, Julia, Tabeling, Christoph, Barbosa-Sicard, Eduardo, Chanson, Marc, Kwak, Brenda R., Shin, Hee-Sup, Wu, Songwei, Isakson, Brant E., Witzenrath, Martin, de Wit, Cor, Fleming, Ingrid, Kuppe, Hermann, and Kuebler, Wolfgang M.

Subjects
Vascular endothelium -- Genetic aspects, Vasoconstriction -- Genetic aspects, Cellular signal transduction -- Genetic aspects, Hypoxia -- Genetic aspects -- Care and treatment, Health care industry
Abstract

Hypoxic pulmonary vasoconstriction (HPV) is a physiological mechanism by which pulmonary arteries constrict in hypoxic lung areas in order to redirect blood flow to areas with greater oxygen supply. Both oxygen sensing and the contractile response are thought to be intrinsic to pulmonary arterial smooth muscle cells. Here we speculated that the ideal site for oxygen sensing might instead be at the alveolocapillary level, with subsequent retrograde propagation to upstream arterioles via connexin 40 (Cx40) endothelial gap junctions. HPV was largely attenuated by Cx40-specific and nonspecific gap junction uncouplers in the lungs of wild-type mice and in lungs from mice lacking Cx40 ([Cx40.sup.-/-]). In vivo, hypoxemia was more severe in [Cx40.sup.-/-] mice than in wild-type mice. Real-time fluorescence imaging revealed that hypoxia caused endothelial membrane depolarization in alveolar capillaries that propagated to upstream arterioles in wild-type, but not [Cx40.sup.-/-], mice. Transformation of endothelial depolarization into vasoconstriction involved endothelial voltage-dependent α1G subtype [Ca.sup.2+] channels, cytosolic phospholipase [A.sub.2], and epoxyeicosatrienoic acids. Based on these data, we propose that HPV originates at the alveolocapillary level, from which the hypoxic signal is propagated as endothelial membrane depolarization to upstream arterioles in a Cx40-dependent manner., Introduction Hypoxic pulmonary vasoconstriction (HPV) is a fundamental physiological mechanism by which the lung optimizes ventilation/perfusion (V/Q) matching, redirecting blood flow from poorly to better ventilated areas (1). Yet in [...]

Published
2012
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36. A quick assay for monitoring recombinant hirudin during cardiopulmonary bypass in patients with heparin-induced thrombocytopenia type IIAdaptation of the ecarin clotting time to the Act II device

Author

Koster, Reas, Loebe, Matthias, Hansen, Roland, Bauer, Mathias, Mertzlufft, Fritz, Kuppe, Hermann, and Hetzer, Roland

Subjects
Coronary artery bypass, Patient monitoring equipment, Anticoagulants (Medicine), Thrombocytopenia, Health
Abstract

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1067/mtc.2000.106088 Byline: reas koster, Matthias Loebe, Roland Hansen, Mathias Bauer, Fritz Mertzlufft, Hermann Kuppe, Roland Hetzer Abstract: Background: Recombinant hirudin is increasingly advocated as a promising alternative anticoagulation for patients with heparin-induced thrombocytopenia type II during cardiopulmonary bypass. This requires monitoring of the ecarin clotting time. No commercial ecarin clotting time assay is available for clinical use. We adapted the ecarin clotting time to the easy-to-handle ACT II device. Methods: Three different concentrations of the ecarin reagent (20, 10, 5 U/mL) were investigated as preliminary studies. Standard calibration curves were constructed for concentrations of recombinant hirudin ranging from 0 to 5 [mu]g/mL. In vivo samples were collected from patients with heparin-induced thrombocytopenia type II who underwent cardiopulmonary bypass, and the values were compared with the values obtained by the chromogenic method. The final concentration for the assay of 5 IU/mL ecarin was further assessed in vitro for reproducibility and the influence of variations in hematocrit, platelet count, and procoagulants. Results: All three concentrations of ecarin revealed linearity to 5 [mu]g/mL concentrations of recombinant hirudin. The ecarin concentration of 5 U/mL revealed the best correlation (0.87) to the laboratory method, was reproducible over the whole recombinant hirudin range, and was not influenced by the variations in the in vitro setup. Conclusions: The ACT II/ecarin clotting time with an ecarin concentration of 5 U/mL is a simple and reliable assay for monitoring recombinant hirudin during cardiopulmonary bypass. Use of this assay allows a wider use of recombinant hirudin in patients with heparin-induced thrombocytopenia type II during bypass and thereby may contribute to the safer management of these patients. (J Thorac Cardiovasc Surg 2000;119:1278-83) Author Affiliation: From the Department of Anesthesiology,.sup.a Deutsches Herzzentrum Berlin; Department of Laboratory Medicine and Pathobiochemistry,.sup.b Campus Rudolf Virchow, Charite, Berlin; Department of Cardiothoracic and Vascular Surgery,.sup.c Deutsches Herzzentrum Berlin; and Department of Anesthesiology and Intensive Care Medicine,.sup.d University of Homburg-Saar, Germany Article History: Received 15 July 1999; Revised 28 October 1999; Revised 13 January 2000; Accepted 1 February 2000 Article Note: (footnote) [star] Address for reprints: Andreas Koster, MD, Deutsches Herzzentrum Berlin, Augustenburgerplatz 1, 13353 Berlin, Germany (E-mail: koster@dhzb.de ).

Published
2000

40. Prophylactic perioperative sodium bicarbonate to prevent acute kidney injury following open heart surgery: a multicenter double-blinded randomized controlled trial

Author

Haase, Michael, Haase-Fielitz, Anja, Plass, Michael, Kuppe, Hermann, Hetzer, Roland, Hannon, Claire, Murray, Patrick T., Bailey, Michael J., Bellomo, Rinaldo, and Bagshaw, Sean M.

Subjects
Heart -- Surgery, Acute renal failure -- Prevention, Sodium bicarbonate -- Health aspects, Pain, Postoperative -- Prevention, Biological sciences
Abstract

Background: Preliminary evidence suggests a nephroprotective effect of urinary alkalinization in patients at risk of acute kidney injury. In this study, we tested whether prophylactic bicarbonate-based infusion reduces the incidence of acute kidney injury and tubular damage in patients undergoing open heart surgery. Methods and Findings: In a multicenter, double-blinded (patients, clinical and research personnel), randomized controlled trial we enrolled 350 adult patients undergoing open heart surgery with the use of cardiopulmonary bypass. At induction of anesthesia, patients received either 24 hours of intravenous infusion of sodium bicarbonate (5.1 mmol/kg) or sodium chloride (5.1 mmol/kg). The primary endpoint was the proportion of patients developing acute kidney injury. Secondary endpoints included the magnitude of acute tubular damage as measured by urinary neutrophil gelatinase-associated lipocalin (NGAL), initiation of acute renal replacement therapy, and mortality. The study was stopped early under recommendation of the Data Safety and Monitoring Committee because interim analysis suggested likely lack of efficacy and possible harm. Groups were non-significantly different at baseline except that a greater proportion of patients in the sodium bicarbonate group (66/174 [38%]) presented with preoperative chronic kidney disease compared to control (44/176 [25%]; p = 0.009). Sodium bicarbonate increased urinary pH (from 6.0 to 7.5, p Conclusions: Urinary alkalinization using sodium bicarbonate infusion was not found to reduce the incidence ofacute kidney injury or attenuate tubular damage following open heart surgery; however, it was associated with a possible increase in mortality. On the basis of these findings we do not recommend the prophylactic use of sodium bicarbonate infusion to reduce the risk of acute kidney injury. Discontinuation of growing implementation of this therapy in this setting seems to be justified. Trial registration: ClinicalTrials.gov NCT00672334, Introduction Acute kidney injury is a global health problem with more than 10 million people affected annually [1]. It is independently related to long-term morbidity [2] and an estimated 4 [...]

Published
2013
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43. Effet de l’inhalation d’iloprost sur le pronostic postopératoire chez les patients chirurgicaux cardiaques à haut risque : une étude multicentrique randomisée et prospective (ILOCARD).

Author

Winterhalter, Michael, Rex, Steffen, Stoppe, Christian, Kienbaum, Peter, Müller, Hans-Helge, Kaufmann, Ines, Kuppe, Hermann, Dongas, Aristidis, Zwissler, Bernhard, and ILOCARD Investigators

Abstract

Copyright of Canadian Journal of Anaesthesia / Journal Canadien d'Anesthésie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2019
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44. Abstract 13135: The Clinical Significance of Intraoperative Iloprost Inhalation on Outcome of High Risk Cardiac Surgical Patients: A Multicenter Randomized Controlled Trial

Author

Winterhalter, Michael, primary, Rex, Steffen, additional, Stoppe, Christian, additional, Kienbaum, Peter, additional, Müller, Hans-Helge, additional, Kaufmann, Ines, additional, Dongas, Aristidis, additional, Kuppe, Hermann, additional, and Zwissler, Bernhard, additional

Published
2016
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45. Effect of iloprost inhalation on postoperative outcome in high-risk cardiac surgical patients: a prospective randomized-controlled multicentre trial (ILOCARD)

Author

Winterhalter, Michael, Rex, Steffen, Stoppe, Christian, Kienbaum, Peter, Müller, Hans-Helge, Kaufmann, Ines, Kuppe, Hermann, Dongas, Aristidis, and Zwissler, Bernhard

Abstract

Purpose: Perioperative right ventricular (RV) failure due to pressure overload from pulmonary hypertension (PH) worsens postoperative outcomes after cardiac surgery. Inhaled iloprost is a potent pulmonary vasodilator improving RV performance, ameliorating myocardial and pulmonary ischemia-reperfusion injury and attenuating inflammation. We hypothesized that the prophylactic inhalation of iloprost would reduce postoperative ventilation times after cardiac surgery. Methods: In this phase III, multicentre, randomized, double-blind, placebo-controlled trial, we randomly assigned 253 cardiac surgical patients at high risk of perioperative RV failure to the prophylactic inhalation of 20 µg iloprost or placebo before and during weaning from extracorporeal circulation. The primary endpoint was the duration of postoperative ventilation. Secondary endpoints included perioperative hemodynamics, intensive care unit and hospital length of stay, and 90-day mortality. Safety was assessed by the incidence of adverse events. Results: Iloprost had no significant effect on the median [interquartile range] duration of postoperative ventilation compared with placebo (720 [470–1170] min vs778 [541–1219] min, respectively; median decrease, 65 min; 95% confidence interval [CI], − 77 to 210; P= 0.37). While the nebulization of iloprost decreased RV afterload and improved cardiac index, major secondary endpoints were not significantly affected. Ninety-day mortality occurred in 14% of the iloprost patients compared with 14% of the placebo patients (hazard ratio, 0.97; 95% CI, 0.50 to 1.89; P= 0.93). The incidence of adverse events was comparable in both groups. Conclusions: The prophylactic inhalation of iloprost did not meaningfully improve the outcome in high-risk cardiac surgical patients. Trial registration: www.clinicaltrials.gov(NCT00927654); registered 25 June, 2009.

Published
2019
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