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101. Hemodynamic responses to mental stress during salt loading

Author

Goyal, Maria Gefke, Christensen, Niels Juel, Bech, Per, Frandsen, Erik, Damgaard, Morten, Asmar, Ali, Norsk, Peter, Goyal, Maria Gefke, Christensen, Niels Juel, Bech, Per, Frandsen, Erik, Damgaard, Morten, Asmar, Ali, and Norsk, Peter

Abstract

PURPOSE: The purpose was to examine whether prolonged moderate stress associated with a student exam would increase the blood pressure response to a salt load in young healthy normotensive individuals.METHODS: Ten healthy young subjects were examined at two different occasions in random order (i) during preparation for a medical exam (prolonged stress) and (ii) outside the exam period (low stress). All subjects consumed a controlled diet for 3 days with low- or high-salt content in randomized order. The subjective stress was measured by Spielberger's State-Trait Anxiety Inventory-Scale, SCL Symptom Checklist for stress and the Visual Analogue Scale. On each level of stress, 24-h ambulatory blood pressure and cardiac output (CO) were measured. Furthermore, plasma norepinephrine (NE), epinephrine (E) and plasma renin activity (PRA) were measured.RESULTS: Twenty-four-hour ABP, 24-h heart rate, CO as well as plasma levels of NE, E and PRA remained unchanged by changes in stress level. Day-night reduction in SAP was significantly larger during moderate stress and high-salt intake; however, no significant difference was observed during daytime and night-time. Individual increase in mental stress correlated significantly with an individual decrease in PRA (SCL-17, r = -0·80, P<0·05, STAIr = -0·64 P<0·05) during high-salt intake.CONCLUSION: Moderate stress over a period of time in young healthy normotensive individuals does not lead to changes in 24-h ABP. However, the augmented reduction in day-to-night systolic blood pressure during high-salt intake and moderate stress may indicate that stress affects blood pressure regulation.

Published
2017

102. Atrial distension, arterial pulsation, and vasopressin release during negative pressure breathing in humans

Author

PUMP, BETTINA, DAMGAARD, MORTEN, GABRIELSEN, ANDERS, BIE, PETER, CHRISTENSEN, NIELS JUEL, and NORSK, PETER

Subjects
Blood pressure -- Physiological aspects, Nervous system, Sympathetic -- Research, Vasopressin -- Physiological aspects, Biological sciences
Abstract

During an antiorthostatic posture change, left atrial (LA) diameter and arterial pulse pressure (PP) increase, and plasma arginine vasopressin (AVP) is suppressed. By comparing the effects of a 15-min posture change from seated to supine with those of 15-min seated negative pressure breathing in eight healthy males, we tested the hypothesis that with similar increases in LA diameter, suppression of AVP release is dependent on the degree of increase in PP. LA diameter increased similarly during the posture change and negative pressure breathing (-9 to -24 mmHg) from between 30 and 31 [+ or -] 1 to 34 [+ or -] 1 mm (P < 0.05). The increase in PP from 38 [+ or -] 2 to 44 [+ or -] 2 mmHg (P < 0.05) was sustained during the posture change but only increased during the initial 5 min of negative pressure breathing from 36 [+ or -] 3 to 42 [+ or -] 3 mmHg (P [is less than] 0.05). Aortic transmural pressure decreased during the posture change and increased during negative pressure breathing. Plasma AVP was suppressed to a lower value during the posture change (from 1.5 [+ or -] 0.3 to 1.2 [+ or -] 0.2 pg/ml, P [is less than] 0.05) than during negative pressure breathing (from 1.5 [+ or -] 0.3 to 1.4 [+ or -] 0.3 pg/ml). Plasma norepinephrine was decreased similarly during the posture change and negative pressure breathing compared with seated control. In conclusion, the results are in compliance with the hypothesis that during maneuvers with similar cardiac distension, suppression of AVP release is dependent on the increase in PP and, furthermore, probably unaffected by static aortic baroreceptor stimulation. antidiuretic hormone; baroreceptors; blood pressure; sympathetic nervous system

Published
2001

103. Central volume expansion is pivotal for sustained decrease in heart rate during seated to supine posture change

Author

PUMP, BETTINA, KAMO, TSUTOMU, GABRIELSEN, ANDERS, BIE, PETER CHRISTENSEN, NIELS JUEL, and NORSK, PETER

Subjects
Blood pressure -- Measurement, Vasopressin -- Physiological aspects, Heart beat -- Measurement, Aortic body reflex -- Testing, Biological sciences
Abstract

During prolonged, static carotid baroreceptor stimulation by neck suction (NS) in seated humans, heart rate (HR) decreases acutely and thereafter gradually increases. This increase has been explained by carotid baroreceptor adaptation and/or buffering by aortic reflexes. During a posture change from seated to supine (Sup) with similar carotid stimulation, however, the decrease in HR is sustained. To investigate whether this discrepancy is caused by changes in central blood volume, we compared (n = 10 subjects) the effects of 10 min of seated NS (adjusted to simulate carotid stimulation of a posture change), a posture change from seated to Sup, and the same posture change with left atrial (LA) diameter maintained unchanged by lower body negative pressure (Sup + LBNP). During Sup, the prompt decreases in HR and mean arterial pressure (MAP) were sustained. HR decreased similarly within 30 s of NS (65 [+ or -] 2 to 59 [+ or -] 2 beats/min) and Sup + LBNP (65 [+ or -] 2 to 58 [+ or -] 2 beats/min) and thereafter gradually increased to values of seated. MAP decreased similarly within 5 min during Sup + LBNP and NS (by 7 [+ or -] 1 to 9 [+ or -] 1 mmHg) and thereafter tended to increase toward values of seated subjects. Arterial pulse pressure was increased the most by Sup, less so by Sup + LBNP, and was unchanged by NS. LA diameter was only increased by Sup. In conclusion, static carotid baroreceptor stimulation per se causes the acute ([is less than] 30 s) decrease in HR during a posture change from seated to Sup, whereas the central volume expansion (increased LA diameter and/or arterial pulse pressure) is pivotal to sustain this decrease. Thus the effects of central volume expansion override adaptation of the carotid baroreceptors and/or buffering of aortic reflexes. antidiuretic hormone; baroreceptors; blood pressure; lower body negative pressure; neck suction

Published
2001

104. Neuroendocrine and renal effects of intravascular volume expansion in compensated heart failure

Author

GABRIELSEN, ANDERS, BIE, PETER, HOLSTEIN-RATHLOU, NIELS HENRIK, CHRISTENSEN, NIELS JUEL, WARBERG, JORGEN, DIGE-PETERSEN, HARRIET, FRANDSEN, ERIK, GALATIUS, SOREN, PUMP, BETTINA, SORENSEN, VIBEKE B., KASTRUP, JENS, and NORSK, PETER

Subjects
Neuroendocrinology -- Research, Heart failure -- Physiological aspects, Kidneys -- Physiological aspects, Water-electrolyte balance (Physiology) -- Research, Biological sciences
Abstract

To examine if the neuroendocrine link between volume sensing and renal function is preserved in compensated chronic heart failure [HF, ejection fraction 0.29 [+ or -] 0.03 (mean [+ or -] SE)] we tested the hypothesis that intravascular and central blood volume expansion by 3 h of water immersion (WI) elicits a natriuresis. In HF, WI suppressed ANG II and aldosterone (Aldo) concentrations, increased the release of atrial natriuretic peptide (ANP), and elicited a natriuresis (P [is less than] 0.05 for all) compared with seated control. Compared with control subjects (n = 9), ANG II, Aldo, and ANP concentrations were increased (P [is less than] 0.05) in HF, whereas absolute and fractional sodium excretion rates were attenuated [47 [+ or -] 16 vs. 88 [+ or -] 15 [micro]mol/min and 0.42 [+ or -] 0.18 vs. 0.68 [+ or -] 0.12% (mean [+ or -] SE), respectively, both P [is less than] 0.05]. When ANG II and Aldo concentrations were further suppressed (P [is less than] 0.05) during WI in HF (by sustained angiotensin-converting enzyme inhibitor therapy, n = 9) absolute and fractional sodium excretion increased (P [is less than] 0.05) to the level of control subjects (108 [+ or -] 34 [micro]mol/min and 0.70 [+ or -] 0.23%, respectively). Renal free water clearance increased during WI in control subjects but not in HF, albeit plasma vasopressin concentrations were similar in the two groups. In conclusion, the neuroendocrine link between volume sensing and renal sodium excretion is preserved in compensated HF. The natriuresis of WI is, however, modulated by the prevailing ANG II and Aldo concentrations. In contrast, renal free water clearance is attenuated in response to volume expansion in compensated HF despite normalized plasma AVP concentrations. renin-angiotensin system; aldosterone; vasopressin; waterelectrolyte balance

Published
2001

105. Endurance training and GH administration in elderly women: effects on abdominal adipose tissue lipolysis

Author

LANGE, KAI HENRIK WIBORG, LORENTSEN, JEANNE, ISAKSSON, FREDRIK, JUUL, ANDERS, RASMUSSEN, MICHAEL HOJBY, CHRISTENSEN, NIELS JUEL, BULOW, JENS, and KJAER, MICHAEL

Subjects
Physical fitness -- Evaluation, Women -- Physiological aspects, Adipose tissues -- Physiological aspects, Lipid metabolism -- Research, Biological sciences
Abstract

In the present study, the effect of endurance training alone and endurance training combined with recombinant human growth hormone (rhGH) administration on subcutaneous abdominal adipose tissue lipolysis was investigated. Sixteen healthy women [age 75 [+ or -] 2 yr (mean [+ or -] SE)] underwent a 12-wk endurance training program on a cycle ergometer. rhGH was administered in a randomized, double-blinded, placebo-controlled design in addition to the training program. Subcutaneous abdominal adipose tissue lipolysis was estimated by means of microdialysis combined with measurements of subcutaneous abdominal adipose tissue blood flow (ATBF; [sup.133]Xe washout). Whole body fat oxidation was estimated simultaneously by indirect calorimetry. Before and after completion of the training program, measurements were performed both at rest and during 60 min of continuous cycling at a workload corresponding to 60% of pretraining peak oxygen uptake. Endurance training alone did not affect subcutaneous abdominal adipose tissue lipolysis either at rest or during exercise, as reflected by identical levels of interstitial adipose tissue glycerol, subcutaneous abdominal ATBF, and plasma nonesterified fatty acids before and after completion of the training program. Similarly, no effect on subcutaneous abdominal adipose tissue lipolysis was observed when combining endurance training with rhGH administration. However, in both the placebo and the GH groups, fat oxidation was significantly increased during exercise performed at the same absolute workload after completion of the training program. We conclude that the changed lipid metabolism during exercise observed after endurance training alone or after endurance training combined with rhGH administration is not due to alterations in subcutaneous abdominal adipose tissue metabolism in elderly women. adipose tissue blood flow; catecholamines; fat metabolism; microdialysis; body composition

Published
2001

106. Cardiovascular effects of static carotid baroreceptor stimulation during water immersion in humans

Author

PUMP, BETTINA, SHIRAISHI, MAKOTO, GABRIELSEN, ANDERS, BIE, PETER, CHRISTENSEN, NIELS JUEL, and NORSK, PETER

Subjects
Carotid artery -- Physiological aspects, Blood pressure -- Measurement, Immersion -- Physiological aspects, Biological sciences
Abstract

We hypothesized that the more-pronounced hypotensive and bradycardic effects of an antiorthostatic posture change from seated to supine than water immersion are caused by hydrostatic carotid baroreceptor stimulation. Ten seated healthy males underwent five interventions of 15-min each of 1) posture change to supine, 2) seated water immersion to the Xiphoid process (WI), 3) seated neck suction (NS), 4) WI with simultaneous neck suction (-22 mmHg) adjusted to simulate the carotid hydrostatic pressure increase during supine (WI + NS), and 5) seated control. Left atrial diameter increased similarly during supine, WI + NS, and WI and was unchanged during control and NS. Mean arterial pressure (MAP) decreased the most during supine (7 [+ or -] 1 mmHg, P [is less than] 0.05) and less during WI + NS (4 [+ or -] 1 mmHg) and NS (3 [+ or -] 1 mmHg). The decrease in heart rate (HR) by 13 [+ or -] 1 beats/min (P [is less than] 0.05) and the increase in arterial pulse pressure (PP) by 17 [+ or -] 4 mmHg (P [is less than] 0.05) during supine was more pronounced (P [is less than] 0.05) than during WI + NS (10 [+ or -] 2 beats/min and 7 [+ or -] 2 mmHg, respectively) and WI (8 [+ or -] 2 beats/min and 6 [+ or -] 1 mmHg, respectively, P [is less than] 0.05). Plasma vasopressin decreased only during supine and WI, and plasma norepinephtine, in addition, decreased during WI + NS (P [is less than] 0.05). In conclusion, WI + NS is not sufficient to decrease MAP and HR to a similar extent as a 15-min seated to supine posture change. We suggest that not only static carotid baroreceptor stimulation but also the increase in PP combined with low-pressure receptor stimulation is a possible mechanism for the more-pronounced decrease in MAP and HR during the posture change. antidiuretic hormone; blood pressure; lower body negative pressure

Published
2001

107. Cardiovascular and neuroendocrine responses to water immersion in compensated heart failure

Author

GABRIELSEN, ANDERS, SORENSEN, VIBEKE B., PUMP, BETTINA, GALATIUS, SOREN, VIDEBAEK, REGITZE, BIE, PETER, WARBERG, JORGEN, CHRISTENSEN, NIELS JUEL, WROBLEWSKI, HENRIK, KASTRUP, JENS, and NORSK, PETER

Subjects
Heart failure -- Physiological aspects, Neuroendocrinology -- Research, Immersion -- Physiological aspects, Vascular resistance -- Measurement, Nervous system, Sympathetic -- Physiological aspects, Renin-angiotensin system -- Physiological aspects, Endothelin -- Physiological aspects, Vasopressin -- Physiological aspects, Biological sciences
Abstract

Gabrielsen, Anders, Vibeke B. Sorensen, Bettina Pump, Soren Galatius, Regitze Videbaek, Peter Bie, Jorgen Warberg, Niels Juel Christensen, Henrik Wroblewski, Jens Kastrup, and Peter Norsk. Cardiovascular and neuroendocrine responses to water immersion in compensated heart failure. Am J Physiol Heart Circ Physiol 279: H1931-H1940, 2000.--The hypothesis was tested that cardiovascular and neuroendocrine (norepinephrine, renin, and vasopressin) responses to central blood volume expansion are blunted in compensated heart failure (HF). Nine HF patients [New York Heart Association class II-III, ejection fraction = 0.28 [+ or -] 0.02 (SE)] and 10 age-matched controls (ejection fraction = 0.68 [+ or -] 0.03) underwent 30 min of thermoneutral (34.7 [+ or -] 0.02 [degrees] C) water immersion (WI) to the xiphoid process. WI increased (P [is less than] 0.05) central venous pressure by 3.7 [+ or -] 0.6 and 3.2 [+ or -] 0.4 mmHg and stroke volume index by 12.2 [+ or -] 2.1 and 7.2 [+ or -] 2.1 ml [multiplied by] [beat.sup.-1] [multiplied by] [m.sup.-2] in controls and HF patients, respectively. During WI, systemic vascular resistance decreased (P [is less than] 0.05) similarly by 365 [+ or -] 66 and 582 [+ or -] 227 dyn [multiplied by] s [multiplied by] [cm.sup.-5] in controls and HF patients, respectively. Forearm subcutaneous vascular resistance decreased by 19 [+ or -] 7% (P [is less than] 0.05) in controls but did not change in HF patients. Heart rate decreased less during WI in HF patients, whereas release of norepinephrine, renin, and vasopressin was suppressed similarly in the two groups. We suggest that reflex control of forearm vascular beds and heart rate is blunted in compensated HF but that baroreflex-mediated systemic vasodilatation and neuroendocrine responses to central blood volume expansion are preserved. sympathetic nervous activity; arginine vasopressin; reninangiotensin system; endothelin; baroreceptors

Published
2000

108. Low LBNP tolerance in men is associated with attenuated activation of the renin-angiotensin system

Author

GREENLEAF, JOHN E., PETERSEN, TRINE WELLOW, GABRIELSEN, ANDERS, PUMP, BETTINA, BIE, PETER, CHRISTENSEN, NIELS JUEL, WARBERG, JORGEN, VIDEBAEK, REGITZE, SIMONSON, SHAWN R., and NORSK, PETER

Subjects
Hormone research -- Physiological aspects, Antihypertensive drugs -- Physiological aspects, Vasopressin -- Physiological aspects, Catecholamines -- Physiological aspects, Renin-angiotensin system -- Physiological aspects, Biological sciences
Abstract

Low LBNP tolerance in men is associated with attenuated activation of the renin-angiotensin system. Am J Physiol Regulatory Integrative Comp Physiol 279: R822-R829, 2000.--Plasma vasoactive hormone concentrations [epinephrine ([p.sub.Epi]), norepinephrine ([p.sub.NE]), ANG II ([p.sub.ANG II]), vasopressin ([p.sub.VF]), endothelin-1 ([p.sub.ET-1]) and plasma renin activity ([p.sub.RA]) were measured periodically and compared during lower body negative pressure (LBNP) to test the hypothesis that responsiveness of the renin-angiotensin system, the latter being one of the most powerful vasoconstrictors in the body, is of major importance for LBNP tolerance. Healthy men on a controlled diet (2,822 cai/day, 2 mmol [multiplied by] kg-1 [multiplied by] [day.sup.-1] [Na.sup.+]) were exposed to 30 min of LBNP from -15 to -50 mmHg. LBNP was uneventful for seven men [25 [+ or -] 2 yr, high-tolerance (HiTol) group], but eight men (26 [+ or -] 3 yr) reached presyncope after 11 [+ or -] 1 min [P [is less than] 0.001, low-tolerance (LoTol) group]. Mean arterial pressure (MAP) did not change measurably, but central venous pressure and left atrial diameter decreased similarly in both groups (5-6 mmHg, by [approximately equals]30%, P [is less than] 0.05). Control (0 mmHg LBNP) hormone concentrations were similar between groups, however, PRA differed between them (LoTol 0.6 [+ or -] 0.1, HiTol 1.2 [+ or -] 0.1 ng ANG I[multiplied by][ml.sup.-1][multiplied by][h.sup.-1], P [is less than] 0.05). LBNP increased (P [is less than] 0.05) [p.sub.RA] and [p.sub.ANG II], respectively, more in the HiTol group (9.9 [+ or -] 2.2 ng ANG I[multiplied by][ml.sup.-1][multiplied by][h.sup.-1] and 58 [+ or -] 12 pg/ml) than in LoTol subjects (4.3 [+ or -] 0.9 ng ANG I[multiplied by][ml.sup.-1][multiplied by][h.sup.-1] and 28 [+ or -] 6 pg/ml). In contrast, the increase in [p.sup.VP] was higher (P [is less than] 0.05) in the LoTol than in the HiTol group. The increases (P [is less than] 0.05) for [p.sub.NE] were nonsignificant between groups, and [P.sub.ET-1] remained unchanged. Thus there may be a causal relationship between attenuated activation of [p.sub.RA] and [p.sub.AN II] and presyncope, with [p.sub.VP] being a possible cofactor. Measurement of resting [p.sub.RA] may be of predictive value for those with lower hypotensive tolerance. hypotensive tolerance; vasopressin; central venous pressure; catecholamines

Published
2000

109. Arterial pulse pressure and vasopressin release during graded water immersion in humans

Author

GABRIELSEN, ANDERS, WARBERG, JORGEN, CHRISTENSEN, NIELS JUEL, BIE, PETER, STADEAGER, CARSTEN, PUMP, BETTINA, and NORSK, PETER

Subjects
Blood pressure -- Research, Nervous system, Sympathetic -- Research, Cardiac output -- Physiological aspects, Vasopressin -- Physiological aspects, Biological sciences
Abstract

Gabrielsen, Anders, Jorgen Warberg, Niels Juel Christensen, Peter Bie, Carsten Stadeager, Bettina Pump, and Peter Norsk. Arterial pulse pressure and vasopressin release during graded water immersion in humans. Am J Physiol Regulatory Integrative Comp Physiol 278: R1583-R1588, 2000.--Previous results indicate that arterial pulse pressure modulates release of arginine vasopressin (AVP) in humans. The hypothesis was therefore tested that an increase in arterial pulse pressure is the stimulus for suppression of AVP release during central blood volume expansion by water immersion. A two-step immersion model (n = 8) to the xiphoid process and neck, respectively, was used to attain two different levels of augmented cardiac distension. Left atrial diameter (echocardiography) increased from 28 [+ or -] 1 to 34 [+ or -] 1 mm (P [is less than] 0.05) during immersion to the xiphoid process and more so (P [is less than] 0.05), to 36 [+ or -] 1 mm, during immersion to the neck. During immersion to the xiphoid process, arterial pulse pressure (invasively measured in a brachial artery) increased (P [is less than] 0.05) from 44 [+ or -] 1 to 51 [+ or -] 2 mmHg and to the same extent from 42 [+ or -] 1 to 52 [+ or -] 2 mmHg during immersion to the neck. Mean arterial pressure was unchanged during immersion to the xiphoid process and increased during immersion to the neck by 7 [+ or -] 1 mmHg (P [is less than] 0.05). Arterial plasma AVP decreased from 2.5 [+ or -] 0.7 to 1.8 [+ or -] 0.5 pg/ml (P [is less than] 0.05) during immersion to the xiphoid process and significantly more so (P [is less than] 0.05), to 1.4 [+ or -] 0.5 pg/ml, during immersion to the neck. In conclusion, other factors besides the increase in arterial pulse pressure must have participated in the graded suppression of AVP release, comparing immersion to the xiphoid process with immersion to the neck. We suggest that when arterial pulse pressure is increased, graded distension of cardiopulmonary receptors modulate AVP release. blood pressure; sympathetic nervous system; baroreceptors; cardiac output

Published
2000

111. Tenth Annual Meeting of the European Association for the Study of Diabetes: Jerusalem, Israel, September 11–13, 1974

Author

Alberti, K. G. M. M., Iversen, J., Christensen, N. J., Andersson, A., Jarrousse, Claire, Andersson, Arne, Hellerström, Claes, Andreani, D., Tamburrano, G., Tamburrano, S., Gambardella, S., Ardill, Joy, Montgomery, D. A. D., Hadden, D. R., Assan, R., Attali, J. R., Selmi, A., Bourdillat, N., Soufflet, E., Girard, J. R., Bajaj, J. S., Chinna, G. S., Garg, S. K., Singh, Baldev, Balasse, E. O., Neef, M. A., Beischer, W., Melani, F., Keller, L., Hinz, M., Kroder, A., Maier, V., Pfeiffer, E. F., Bendayan, M., Sandborn, E., Rasio, E., Bensoussan, D., Levy-Toledano, S., Passa, P., Caen, J., Berger, M., Goodman, M. N., Hagg, S. A., Ruderman, N. B., Beyer, J., Cordes, U., Travniczek, H., Heider, W., Schöffling, K., Happ, J., Grimm, H., Pünchera, W., Althoff, P. H., Fröhlich, A., Bianco, A. R., Schwartz, R. H., Handwerger, B. S., Blackshear, P. J., Holloway, P. A. H., Williamson, D. H., Boquist, L., Hellman, Bo, Lernmark, Åke, Täljedabl, Inge-Bert, Bottermann, P., Schweigart, U., Zilker, Th., Hansen, W., Brachet, E., Rogister, C., Broer, Y., Freychet, P., Rosselin, G., Brunengraber, H., Vertongen, F., Boutry, M., Camu, F., Christacopoulos, P., Karamanos, B., Papadimitriou, P., Kardatos, Ch., Christensen, Niels Juel, Neubauer, Bent, Christophe, Jean, Winand, Jacques, Dehaye, Jean, Cuendet, G. S., Loten, E. G., Jeanrenaud, B., Davis, E., Yodaiken, Ralph E., Yanko, L., Herman, J. B., Garcia, S. Duran, Jarrousse, C., Ditzel, J., Daugaard, Niels Peters, Andersen, Haakon, Egeberg, J., Nerup, J., Andersen, O. O., Kromann, H., Bendixen, G., Poulsen, J. E., Eschwege, E., Falkmer, S., Emdin, S. O., Havu, N., Biuw, L. Winbladh, Sundby, F., Cutfield, J. F., Cutfield, S. M., Dodson, G. G., Peterson, J. D., Steiner, D. F., Fallucca, F., Menzinger, G., Iavicoli, M., Federspil, G., de Palo, C., Zago, E., Casara, D., Zaccaria, M., Scandellari, C., Felber, J. -P., Magnenat, G., Curchod, B., Pittet, Ph., Lytras, N., Müller-Hess, R., Geser, C. A., Jéquier, E., Flanagan, R. W. J., Buchanan, K. D., Murphy, R. F., Fölling, Ivar, Fromantin, M., Freyria, J., Bressac, F., Geisthövel, W., Niedergerke, U., Morgner, K. D., Willms, B., Mitzkat, H. J., Gey, K. F., Bühler, E., Sommer, P., Gey, K. F., Georgi, H., Sommer, P., Lengsfeld, H., Ghiea, D., Costiner, E., Simionescu, L., Oprescu, M., Grill, V., Cerasi, E., Gundersen, H. J. G., Gutman, A., Adler, J., Bar-Or, D., Gutzeit, A., Cerasi, E., Guy-Grand, B., Bigorie, B., Gylfe, Erik, Idahl, Lars-Åke, Hamosh, Margit, Hamosh, Paul, Hart, Adrian, Cohen, H., Thorp, J. M., Hedeskov, C. J., Capito, K., Forruby, B., Henquin, J. C., Lambert, A. B., Lambert, A. E., Henquin, J. C., Hepp, K. D., Renner, R., Häring, H. U., Mehnert, H., Kemmler, W., Löffler, G., Mehnert, H., Herchuelz, A., Mahy, M., Herrera, Emilip, Garcia-Rafanell, J., Morell, J., Heuclin, Ch., Attali, J. R., Girard, J. R., Assan, R., Hicks, B. H., Taylor, C. I., Vij, S. K., Pek, S., Knopf, R. F., Floyd, Jr., J. C., Fajans, S. S., Hockaday, T. D. R., Hockaday, J. M., Mann, J. I., Turner, R. C., Hockaday, T. D. R., Honour, A. J., Ikeda, Y., Saito, S., Matsuura, Y., Obayashi, N., Morimoto, Y., Sano, T., Abe, M., Jacouot, R., Felix, J. M., Legrele, C., Sutter-Dub, M. -Th., Sutter, B. Ch. J., Kammerer, L., Fehér, J., Lévai, J., Dénes, R., Stützel, M., Balázsi, I., Láng, I., Littmann, L., Karakash, C., Assimacopoulos, F., Katsilambros, N., Papadopoulos, G., Varonos, D., Daikos, G., Keen, H., Jarrett, R. J., Fuller, J. H., Kiesselbach, N. H. K., Puls, W., Keup, U., Kikkawa, Ryuichi, Duvillard, D., Ravazzola, M., Stauffacher, W., Köbberling, J., Kattermann, R., Kobberling, J., Creutzfeldt, W., Kohner, Eva M., Hamilton, A. M., Joplin, G. F., Blach, R. K., Fraser, T. R., Kolb, H. J., Weiss, L., Wieland, O. H., Korn, A., Waldhäusl, W., Bonelli, J., Magometsohnigg, D., Hitzenberger, G., Kramp, Robert C., Kremer, G. J., Atzpodien, W., Schnellbacher, B., Krug, B., Mialhe, P., Gross, R., Landgraf, R., Landgraf-Leurs, M., Klingenburg, M., Melamed, I., Hörl, R., Jun, István Láng, Littmann, László, Stützel, Mária, Balázsi, Imre, Langslow, Derek R., Buchanan, Keith D., Freeman, Barry M., Berezin, Meir, Mincu, I., Dumitrescu, C., Ionescu-Tirgoviste, C., Mihalache, N., Boboia, D., Stanescu, J., Ghise-Beer, E., Georgescu, St., Bruckner, I., Popa, I., Muggeo, M., Tiengo, A., Padovan, D., Molinari, M., Müller, Walter A., and Sharp, Geoffrey W. G.

Published
1974
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113. Seventh Annual Meeting of the European Association for the Study Of Diabetes Southampton, England, September 15–17, 1971 Abstacts, Part 1

Author

Aboulker, J. P., Valleron, A. J., Papoz, L., Rathery, M., Adams, P. W., Munday, M. J., Oakley, N. W., Wynn, V., Andreani, D., Fallucca, F., Stirati, G., Tamburrano, G., Cinotti, G. A., Andreev, D., Tarkolev, N., Ditzov, S., Pencev, I., Ancreev, D., Sirskov, L., Arnold, R., Creutzfeldt, C., Deuticke, U., Frerichs, H., Track, N. S., Creutzfeldt, W., Asmal, A. C., Butterfieid, W. J. H., Karamanos, B., Whichelow, M. J., Butterfield, W. J. H., Cox, B. D., Ashcroft, S. J. H., Bassett, J. M., Randle, P. J., Asplund, K., Hellerström, C., Brolin, S. E., Berne, C., Edwards, John C., Petersson, B., Taylor, K. W., Assan, R., Hanoune, J., Attali, J. B., Tchobroutsky, G., Gross, G., Assimacopoulos, F., Orci, L., Rouiller, Ch., Jeanrenaud, B., Cameron, D. P., Amherdt, M., Mira, F., Stauffacher, W., Heindel, J. J., Cushman, S. W., Austoni, M., Federspil, G., Casara, D., Sieolo, N., Scandellari, C., Mastrogiacomo, I., Aynsley-Green, A., Alberti, K. G. M. M., Bacanu, Gh., Stoichescu, L., Nistor, F., Turcanu, V., Anghelescu, L., Bacchus, R. A., Meade, L. G., London, D. R., Baiasse, E. O., Barta, L., Brooser, G., Molnár, Maria, Belfiore, F., Vecchio, L. Lo, Napoli, E., Beyer, J., Cordes, U., Sell, G., Krall, N., Schöffling, K., Biebuyck, J. F., de Haan, B. Bierens, Scherrer, J. R., Pometta, D., Björntorp, P., Sjöström, L., Blach, R. K., Cheng, Hung, Bloom, S. R., Bojanowicz, K., Boquist, L., Brachet, E., Bruni, B., Capra, E., Büber, V., Felber, J. P., Buchanan, K. D., Connon, J. J., Buckle, R. M., Campeami, S., Campeanu, L., Ionesou, M., Cerasi, E., Luft, R., Efendic, S., Chabot, V., Gomez, F., Chiumello, G., del Guercio, M. J., Carnelutti, M., Christensen, Niels Juel, Iversen, J., Christiansen, Aa. Hein, Rasmussen, S. Munkgaard, Vø1und, Aa., Vólund, Aa., Clausen, T., Czyzyk, A., Szadkowski, M., Rogala, H., Lawecki, J., Davies, W. H., Martin, L. B., Mills, J. G., Vardey, C. J., Deckert, T., Lauridsen, U. Birk, Linde, J., Madsen, S. Nistrup, De Leeuw, I., Middelheim, A. Z., de Mowbray, R. R., Turner, J. J., Garner, S. D., Bruck, E., Nye, L., Triggs, S., Devlin, J. G., Varma, M., Kuti, J., Dumitrescu, C., Bolea-Feldman, M., Eschwege, E., Warnet, J. M., Richard, J. L., Menzinger, G., Javicoli, M., Fankhauser, S., Michl, J., Piemonte, G., Sicolo, N., Frezzato, S., Reffo, G. C., Luyckx, A., Lefebvre, P., Zaccaria, M., De Palo, C., Fernandes-Cruz, Jr., A., Lopiz-Quijada, C., Fernandez-Cruz, Jr., A., Otero, M. Luque, Fiedler, H., Hahn, H. J., Ziegler, Brigitte, Ziegler, M., Jutzi, E., Michael, R., Fischer, U., Hommel, H., Bibergeil, H., Förster, O., Rippel, W., Rudas, B., Franckson, J. R. M., Vanroux, R., Leclercq, R., Brunengraber, H., Ooms, H., Freytag, G., Klöppel, G., Fussgänger, R. D., Goberna, R., Schröder, K. E., Laube, H., Pfeiffer, E. F., Gazzola, G. C., Franchi, R., Ronchi, P., Saibene, E., Guidotti, G. G., Geldermans, C., Terpstra, J., Krans, H. M. J., Geser, C. A., Rattenhuber, E., Girard, J., Bal, D., Gligore, V., Mosora, N., Fekete, T., Beraru, T., Pipilian, V. V., Olteanu, L., Serban, A., Calusera, I., Holan, T., Miclutia, M., Gnudi, A., Coscelli, C., Ballerio, G., Palmari, V., Alpi, O., Cavazzini, G., Jéquier, E., Goth, E., Fövenyi, J., Hegedüs, A., Greco, A. V., Ghirlanda, G., Fedeli, G., Fenici, R., Gambassi, G., Grüneklee, D., Hessing, J., Daweke, H., Herberg, L., Gries, F. A., Guder, W., Wieland, O., Guillon, J., Bodic, L., Charbonnel, B., Hadden, D. R., Montgomery, D. A. D., Mayne, Elizabeth, Weaver, J. A., George E, Hahn, J., Richter, O., Steinhilber, S., Kerp, L., Heaney, S. J., Varma, S. K., Whyte, W. G., Walker, R. S., Hepp, K. D., Hellman, B., Lernmark, A., Sehlin, J., Täljedal, I. -B., Hinz, M., Katsilambros, N., Rahman, Y. Abdel, Schatz, H., Maier, V., Schröder, B., Howells, D. P. M., Jackson, R. A., Perry, G., Rogers, J., Advani, U., Jafflol, C., Baldet, L., Vierne, Y., Mirouze, J., Jansen, F. K., Jarrett, R. J., Keen, H., Kaeding, A., Kaffarnik, H., Heink, U., Gassel, W. D., Zöfel, P., Mylarch, K., Keller, U., and Froesch, E. R.

Published
1971
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114. Eighth annual meeting of the European Association for the Study of Diabetes: Madrid, Spain September, 6–8, 1972

Author

Alberti, K. G. M. M., Darley, J., Emerson, Pauline M., Hockaday, T. D. R., Amherdt, M., Like, A. A., Blondel, B., Marliss, B., Wollheim, C., Orci, L., Andersen, O. Ortved, Andersson, Arne, Antonini, F. M., Fumagalli, C., Petruzzi, E., Bertini, G., Mori, S., Tinti, P., Ashcroft, S. J. H., Weerasinghe, L. C. C., Randle, P. J., Assan, R., Slusher, N., Guy-Grand, B., Girard, F., Soufflet, E., Attali, J. R., Ballerio, G., Boillot, J., Atkins, T., Matty, A. J., Bailey, C. J., Aynsley-Green, A., Bloom, S. R., Bacchus, R. A., Meade, L. G., London, D. R., Balant, L., Zahnd, G., Petitpierre, B., Fabre, J., Balasse, E. O., Neef, M. A., Barta, L., Brooser, G., Molnar, Maria, Bataille, D. P., Freychet, P., Kitabgi, P., Rosselin, G. E., Berne, Christian, Beyer, J., Cordes, U., Sell, G., Rosak, C., Schöffling, K., Birkner, B., Henner, J., Wagner, P., Erhardt, F., Dieterle, P., Bloom, S. R., Vaughan, N. J. A., Edwards, A. V., Boquist, L., Brand, I., Söling, H. D., Brandenburg, D., Gliemann, J., Ooms, H. A., Puls, W., Wollmer, A., Camerini-Davalos, R. A., Bloodworth, Jr., J. M. B., Limburg, B., Oppermann, W., Campbell, A. K., Siddle, K., Cañadell, J. M., Barraquer, J., Muiños, A., Heredia, C. D., Castillo-Olivares, J., Guijo, J., Pallardo, L. F., Cerasi, E., Efendić, S., Luft, R., Cerasi, E., Wahren, J., Luft, R., Felig, P., Christensen, Niels Juel, Christiansen, A. H., Vølund, A., Connon, J. J., Trimble, E., Copinschi, G., Leclercq, R., Bruno, O. D., Cordes, U., Sell, G., Beyer, J., Haupt, E., Schöffling, K., Creutzfeldt, C., Track, N. S., Cuendet, G. S., Wollheim, C. B., Cameron, D. P., Balant, L., Stauffacher, W., Marliss, E. B., Czyzyk, A., Lao, B., Bartosiewicz, W., Szczepanik, Z., De Nobel, E., Laar, A. Van't, Koene, R. A. P., Benraad, Th. J., Dietze, G., Hepp, K. D., Wickmayr, M., Mehnert, H., Dixon, K., Exon, P. D., Hughes, H. R., Jones, D. W., Elkeles, R. S., Exon, P. D., Dixon, K., FitzGerald, M. G., Malins, J. M., Falorni, A., Massi-Benedetti, F., Gallo, G., Maffei, S., Fedele, D., Tiengo, A., Muggeo, M., Fabris, P., Crepaldi, G., Federlin, K., Helmke, K., Slijepčević, M., Pfeiffer, E. F., Felber, J. P., Oulès, J., Schindler, Ch., Chabot, V., Fernandez-Cruz, Jr., A., Catalán, E., Otero, M. Luque, Hermida, O. Garcia, Otero, M. Luque, Catalán, E., Flatt, J. P., Blackburn, G., Randers, G., Förster, H., Hoos, I, Lerche, D., Förster, H., Hoos, I., Matthäus, M., Franckson, J. R. M., Ooms, H. A., Frerichs, H., Daweke, H., Gries, F., Grüneklee, D., Hessing, J., Jahnke, K., Keup, U., Miss, H., Otto, H., Puls, W., Schmidt, D., Zumfelde, C., Funcke, H. v., Löffler, G., Wieland, O., Galton, D. J., Guttman, R., Gazzola, G. C., Franchi, R., Ronchi, P., Saibene, V., Guidotti, G. G., Gligore, V., Hîncu, N., Tecuceanu, Rodica, Goberna, R., Garcia-Albertos, F., Tamarit-Rodriguez, J., del Rio, E., Roca, R., Gomez-Acebo, José, Creco, A. V., Fedeli, G., Ghirlanda, G., Fenici, R., Lucente, M., Gutman, A., Agam, G., Nahas, N., Cazalis, P., Gylfe, E., Hellman, B., Hadden, D. R., Connolly, J. H., Montgomery, D. A. D., Weaver, J. A., Hellerström, Claes, Howell, Simon, Andersson, Arne, Edwards, John, Sehlin, J., Täljedal, I. -B., Heptner, W., Neubauer, H. B., Herchuelz, A., Pipeleers, D. G., Malaisse, W. J., Herrera, E., Montoya, Eladio, Hommel, H., Fischer, IT., Schmid, B., Fiedler, H., Bibergeil, H., Iversen, J., Iynedjian, P. B., Peters, G., Jacquemin, C., Lambert, B., Sutter, B. Ch. J., Jakob, A., Zapf, J., Froesch, E. R., Jansen, F. K., Freytag, G., Herberg, L., Jarrett, R. J., Baker, I. A., Jarrousse, C., Rancon, F., Rosselin, G. E., Job, D., Tchobroutsky, G., Eschwege, E., Guyot-Argenton, C., Aubry, J. P., Déret, M., Karman, H., Mialhe, P., Kissebah, A., Tulloch, B., Fraser, Russell, Kissebah, A., Tulloch, B., Vydelingum, N., Fraser, Russell, Kissing, J., Raptis, S., Dollinger, H., Faulhaber, J., Rothenbuchner, G., Pfeiffer, E. F., Kleineke, J., Sauer, H., Söling, H. D., Kloeze, J., Kohner, Eva M., Sutcliffe, Barbara A., Tudball, M., Dollery, C. T., Korp, W., Neubert, J., Bruneder, H., Lenhardt, A., Levett, R. E., Koschinsky, T., Gries, F. A., Landgraf-Leurs, M. M. C., Landgraf, R., Hörl, R., Langslow, D. R., Laube, H., Fussgänger, R., Mayer, R., Pfeiffer, E. F., Laube, H., Fussgänger, R., Klör, H., Pfeiffer, E. F., Lázaro, E., Leclercq-Meyer, V., Marchand, J. J., Malaisse, W., Ledet, Thomas, Lefébvre, P. J., Luyckx, A. S., Le Marchand, Y., Assimacopoulos, F., Singh, A., Amherdt, M., Rouiller, Ch., Jeanrenaud, B., Lenti, G., Frezzotti, R., Angotzi, G., Bardelli, A. M., Pagano, G., Basetti-Sani, A., Galli, M., Lernmark, Å., Fex, G., Lindsay, D. G., Loge, O., Lopez-Quijada, C., Chiva, L., Rodriguez-Lopez, M., Loten, E. G., Loubatières, A. L., Loubatières-Mariani, M. M., Ribes, G., Chapal, J., Lubetzki, J., Duprey, J., Sambourg, Cl., Lefebvre, P. J., Maier, V., Hinz, M., Schatz, H., Nierle, C., Pfeiffer, E. F., Malaisse, W. J., Pipeleers, D. G., Malaisse-Lagae, F., Orci, L., Malaisse-Lagae, F., Amherdt, M., Ravazzola, M., Stauffacher, W., Orci, L., Renold, A. E., Manzano, P., Rojas-Hidalgo, E., Marco, J., Diaz-Fierros, D., Calle, C., Roman, D., Villanueva, M. L., Valverde, I., Marliss, E. B., Wollheim, C. B., Blondel, B., Orci, L., Like, A., Amherdt, M., Stauffacher, W., Massi-Benedetti, F., Luycks, A. L., Fracassini, F., Lefebvre, P. J., Falorni, A., Menzel, R., Michaelis, D., Neumann, I., Bibergeil, H., Schulz, B., Wilke, W., Wulfert, P., Krämer, K., Menzinger, G., Fallucca, F., Tamburrano, F., Carratu', R., Andreani, D., Metzger, P., Franken, P., Balasse, E. O., Michael, R., Hildmann, W., Jutzi, E., Michl, J., Fankhauser, S., Schlichtkrull, J., Mirouze, J., Orsetti, A., Vierne, Y., Arnoux, N., Mølsted-Pederson, L., Tygstrup, Inge, Villumsen, Åge L., Pedersen, Jørgen, Montague, W., Howell, S. L., Moody, A. J., Agerbak, G. S., Sundby, F., Muggeo, M., Crepaldi, G., Fedele, D., Baritussio, A., Naeser, Peter, Navalesi, R., Pilo, A., Lenzi, S., Cecchetti, P., Corsini, G., Donato, L., Nerup, J., Andersen, O. Ortved, Bendixen, G., Egeberg, J., Poulsen, J. E., Nielsen, J. Høiriis, Hansen, F. Mølgaard, Gliemann, J., Niki, A., Niki, H., Koide, T., Lin, B. J., Nikkels, R. E., Terpstra, J., Gay, A., Oakman, R. H., Lazarus, Norman R., Orci, L., Amherdt, M., Stauffacher, W., Like, A. A., Rouiller, C., Renold, A. E., Malaisse-Lagae, F., Ravazzola, M., Ostman, J., Backman, L., Cerasi, E., Luft, R., Hallberg, D., Ostrowski, K., Panten, U., Christians, J., Parving, H. -H., Rasmussen, S. Munkgaard, Marichal, M., Platilovà, H., Dufek, M., Konopàsek, E., Pozuelo, V., Tamarit, J., Suner, A., Castell, C., Pruett, E. D. R., Maehlum, S., Raptis, S., Grebe, B., Chrissiku, M., Rothenbuchner, G., Müller, R., Hinze, H. J., Pfeiffer, E. F., Reinauer, H., Müller-Ruchholtz, E. R., Rietzler, X., Passa, P., Canivet, J., Schatz, H., Otto, J., Hinz, M., Maier, V., Nierle, C., Behrens, G., Bücher, T., Pfeiffer, E. F., Schlumpf, U., Morell, B., Zingg, A., Schönborn, J., Westphal, P., Panten, U., Bloom, G. D., Idahl, L. -A., Lernmark, A., Söderberg, M., Rios, M. Serrano, Hawkins, F. G., Escobar, F., Mato, J. M., Larrodera, L., de Oya, M., Rodriguez-Miñon, J. L., Shafrir, E., Gutman, A., Sitbon, G., Mialhe, P., Skrabalo, Z., Panajatović, N., Papić, Z., Posinovec, J., Stavljenić, A., Lipovac, V., Aganović, I., Soler, N. G., Bennett, M. A., Söling, H. D., Peters, H., Janson, G., Sönksen, P. H., Srivastava, M. C., Tompkins, C. V., Nabarro, J. D. N., Sørensen, N. Schwartz, Ladefoged, K., Wildenhoff, K. E., Sorge, F., Diehl, H. -J., Hoffmann, H., Schwartzkopff, W., Standl, E., Kolb, H., Standl, A., Mehnert, H., Sutherland, H. W., Stowers, J. M., Whetham, J. C. G., Sutter, B. C. J., Billaudel, B., Sutter, B. Ch. J., Sutter-Dub, M. T., Leclercq, R., Jacquot, R., Täljedal, I. B., Tamarit, J., Tamarit-Rodriguez, J., Goberna, R., Gobema, R., Tamás, Jr., Gy., Baranyi, Éva, Baranyi, A., Radvanyi, A., Tatoń, J., Hinek, A., Wiśniewska, A., Tattersall, R. B., Pyke, D. A., Terpstra, J., Slot, J. Bruins, Sande, P. L. M. v. d., Radder, J. K., Waldeok, K. J. J., Muijden, R. C. P. A. v., Tiengo, A., Assan, R., Frerichs, H., Creutzfeldt, W., Turner, D. S., Baker, R. W., Gent, W. G. L., Shabaan, A., Marks, V., Young, D. A. B., Vague, Ph., Heim, H., Laval, C. Martin, Vegezzi, M., Campo, C.Di, Rahamandridona, G., Garron, D., Heyraud, B., Vague, J., Valverde, I., Villanueva, M. L., Lozano, I., Diaz-Fierros, M., Marco, J., Van Assche, F. A., Gepts, W., Van Obberghen, E., Somers, G., Devis, G., Vaughan, G. D., Malaisse-Lagae, F., Orci, L., Malaisse, W. J., Veleminsky, J., Spirova, E., Waldhäusl, W., Frisch, H., Haydl, H., Weiss, L., Löffler, G., Wieland, O., Willms, B., Deuticke, U., Wollheim, C. B., Marliss, E. B., Blondel, B., Orci, L., Like, A., Renold, A. E., Zrůstová, M., and Roštlapil, J.

Published
1973
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115. Kirurgisk Kompendium kittelbog

Author

Ainsworth, Alan Patrick, Alsbjørn, Bjarne, Bardram, Linda, von Buchwald, Christian, Christensen, Niels Juel, Christiansen, Peer Michael, Dahl, Benny, Dalsgaard, Torur, Drzewiecki, Krzysztof Tadeusz, Elung-Jensen, Thomas, Eskesen, Vagn, Fischer, Anders, Gehrchen, Martin, Gjerris, Flemming, Hede, Adam, Hermann, Gregers, Ifaoui, Inge Bøtker-Rasmussen, Iversen, Peter, Jørgensen, Troels Munch, Klarskov, Peter, Knigge, Ulrich, Krag, Christen, Krogsgaard, Michael Rindom, Kroman, Niels Thorndahl, Kroman-Andersen, Bjarne, Larsen, Claus Falck, Larsen, Erik Højkjær, Laurberg, Søren, Lauritzen, Jes Bruun, Leicht, Pernille, Meisner, Søren, Meyhoff, Hans-Henrik, Moesgaard, Flemming Arlee, Mynster, Tommie, Nordling, Jørgen, Nørby, Bettina, Nørgaard, Peter, Olsen, Peter Skov, Osther, Palle J., Ottesen, Bent Smedegaard, Petersen, Michael Mørk, Qvist, Niels, Ravn, Jesper Bohsen, Rosenberg, Jacob, Siim, Elsebeth, Sillesen, Henrik, Steven, Kenneth, Svendsen, Lars Bo, Sønksen, Jens, Sørensen, Anne Marie, Tøttrup, Anders, Walter, Steen, Wara, Pål Edvard, Svendsen, Lars Bo, Nordling, Jørgen, Dahl, B., and Hillingsø, Jens G.

Published
2011

116. Neuroendocrine Responses to Food Intake and Hypoglycemia Decrease Within the First Year After Diagnosis of Type 1 IDDM

Author

HILSTED, JANNIK, DAMHOLT, METTE BRIMNES, and CHRISTENSEN, NIELS JUEL

Subjects
Research, Diabetes research, Diabetes -- Research
Abstract

Neuroendocrine responses (Epinephrine, Norepinephrine and Pancreatic Polypeptide (PP)) to food intake and hypoglycemia are diminished in long-term diabetic patients. In order to establish whether such changes in neuroendocrine responses occur [...]

Published
1999

120. List of Contributors

Author

AGID, R., primary, AMHERDT, M., additional, ANDERSON, P.J., additional, BENNETT, PETER H., additional, BIERMAN, EDWIN L., additional, BIHARI-VARGA, MAGDOLNA, additional, BIRK, J., additional, BISCHOFF, A., additional, BJÖRKERUD, SÖREN, additional, BLOCK, WALTER D., additional, BLOODWORTH, J.M.B., additional, BROSNAN, MARGARET E., additional, CAMERINI-DÁVALOS, RAFAEL A., additional, CAMERON, D.P., additional, CHRISTENSEN, NIELS JUEL, additional, CHURG, JACOB, additional, CIBEIRA, JOSE B., additional, CLAUSS, ROY H., additional, CLEMENTS, REX S., additional, COLE, HAROLD S., additional, CONN, J.W., additional, CRAWFORD, DEREK, additional, CROSSLEY, HAROLD L., additional, DANTA, GYTIS, additional, DEPPERMANN, DIETER, additional, DESCHNER, WENDEL, additional, DULIN, W.E., additional, EHRENREICH, THEODORE, additional, ELASHOFF, ROBERT, additional, ELKELES, R.S., additional, ELLENBERG, MAX, additional, ENGERMAN, R.L., additional, EPSTEIN, FREDERICK H., additional, ESPINOZA, TANYA, additional, FAERMAN, ISAAC, additional, FAJANS, STEFAN S., additional, FAULHABER, J.D., additional, FELDMAN, ROBERT, additional, FLOYD, JOHN C., additional, FOX, DORA, additional, FRASER, RUSSELL, additional, FUCHS, ERHARD, additional, FULLER, GEORGE C., additional, FULLER, J.H., additional, GABBAY, KENNETH H., additional, GARCIA, MARIANO, additional, GERŐ, S., additional, GERRITSEN, G.C., additional, GLASS, ALVIN, additional, GLOCER, LETICIA, additional, GORDON, ARTHUR L., additional, GORDON, TAVIA, additional, HOET, J.J., additional, IBRAHIM, I.I., additional, IWATSUKA, HISASHI, additional, JADZINSKY, MAURICIO N., additional, JARRETT, R.J., additional, JOHANSEN, KLAUS, additional, KANNEL, WILLIAM B., additional, KEEN, H., additional, KEFALIDES, NICHOLAS A., additional, KELLOGG, ANNE, additional, KILO, CHARLES, additional, KINGSBURY, KENNETH J., additional, KNOPF, R.F., additional, KUTHAN, FRANTISEK, additional, LAMPHIEAR, DONALD E., additional, LAUBE, H., additional, LAZAROW, ARNOLD, additional, LEUENBERGER, P., additional, LEWIS, B., additional, LIMBURG, BALDUR, additional, LOWY, C., additional, LUNDBAEK, KNUD, additional, LUYCKX, A.S., additional, McMILLAN, DONALD E., additional, McNAMARA, PATRICIA, additional, MAHLER, ROBERT, additional, MANCINI, M., additional, MARBLE, ALEXANDER, additional, MARQUIÉ, G., additional, MERIMEE, THOMAS J., additional, MILLER, MAX, additional, MORRISON, ANTHONY D., additional, Moss, J.M., additional, OPPERMANN, WERNER, additional, ORCI, L., additional, ØSTERBY, RUTH, additional, OSTRANDER, LEON D., additional, O'SULLIVAN, J.B., additional, PAASIKIVI, J., additional, PAL, S., additional, PATEL, DHANOO, additional, PEK, SUMER, additional, PFEIFFER, E.F., additional, PFEIFFER, MARGRET, additional, POMETTA, D., additional, PRCHKOV, V.K., additional, PREMACHANDRA, B.N., additional, PROUT, THADDEUS E., additional, REDISCH, WALTER, additional, REXROTH, WALTER, additional, ROTHENBUCHNER, G., additional, ROUEN, LAWRENCE R., additional, RUFENER, C., additional, SCHERRER, J.R., additional, SCHLEYER, M., additional, SCHOR, STANLEY S., additional, SCHROEDES, K.E., additional, SIPERSTEIN, MARVIN D., additional, SIREK, ANNA, additional, SIREK, O.V., additional, ŠKRABALO, ZDENKO, additional, SOELDNER, J.S., additional, SORET, M.G., additional, SPIRO, ROBERT G., additional, STAUFFACHER, W., additional, STOUT, ROBERT W., additional, STOWERS, JOHN M., additional, SUSUKI, YASUNOSUKE, additional, TERRY, ERWIN N., additional, VELASCO, CARLOS, additional, VIRÁG, S., additional, VOGLER, NANCY J., additional, VOLK, BRUNO W., additional, WAHL, PETER, additional, WARD, J.D., additional, WEISSMAN, PETER N., additional, WELLMANN, KLAUS F., additional, WILLIAMSON, JOSEPH R., additional, WILLIS, PARK W., additional, WINEGRAD, ALBERT I., additional, YODAIKEN, RALPH E., additional, and YOKOTE, MOTOYOSHI, additional

Published
1973
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125. Decrease in TSH Receptor Autoantibodies during Antithyroid Treatment:Relationship with a Long Noncoding Heg RNA and Cdk1 mRNA in Mononuclear Cells

Author

Christensen, Niels Juel, Habekost, Gurli, Bratholm, Palle, Christensen, Niels Juel, Habekost, Gurli, and Bratholm, Palle

Abstract

We have previously shown that a long noncoding RNA transcript Heg is negatively correlated with TSH receptor autoantibodies (TRAb) in patients with untreated Graves' disease and with CD14 mRNA in treated patients and controls. Thus patients with high concentrations of Heg RNA have low levels of TRAb or CD14 mRNA, respectively. Here we show that an additional factor, gene expression of Cdk1 in mononuclear cells, is positively related to concentrations of TRAb in patients with untreated Graves' disease. Cdk1 mRNA is very important for regulation of cell cycle activity. It is well known that TRAb decrease significantly during treatment with antithyroid drugs. This decrease during treatment cannot be explained by Heg RNA, which remains unchanged. Cdk1 mRNA decreased significantly during treatment to values below values obtained in normal subjects. Thus both Heg RNA and Cdk1 mRNA may influence the level of TSH receptor autoantibodies but by different mechanisms.

Published
2011

127. The paradox of systemic vasodilatation and sympathetic nervous stimulation in space

Author

Norsk, Peter, Christensen, Niels Juel, Norsk, Peter, and Christensen, Niels Juel

Abstract

Udgivelsesdato: 2009-Oct, Cardiac output is increased by some 18% by weightlessness during the initial week of spaceflight compared to upright standing or sitting on the ground and more so during the initial days of flight than at the end. In addition, mean 24-h diastolic, but not systolic pressure, is significantly decreased by 5mmHg. This is in accordance with observations that very acute weightlessness during parabolic airplane flights and a week of weightlessness in space leads to a decrease in systemic vascular resistance. That the arterial resistance vessels are dilated in space is in contrast to the augmented sympathetic nervous activity and decreased urine production, which have consistently been observed in astronauts in space. These contrasting observations require further investigation.

Published
2009

128. A RNA transcript (Heg) in mononuclear cells is negatively correlated with CD14 mRNA and TSH receptor autoantibodies

Author

Habekost, G., Bratholm, P., Christensen, Niels Juel, Habekost, G., Bratholm, P., and Christensen, Niels Juel

Abstract

During a study of gene expression of foxp3 in blood mononuclear cells we observed a DNA product of an unknown RNA fragment. The area of this peak correlated with CD14 mRNA in a small group of subjects. The sequence was localized to chromosome 1. We tested the hypothesis that gene expression of the poly A(-) transcript (designated Heg) in mononuclear cells was correlated with CD14 mRNA in normal subjects and with CD14 mRNA and TSH receptor autoantibodies in patients with acute and untreated Graves' disease. mRNA was expressed in amol/mu g DNA. The main study groups were: (i) normal subjects; (ii) patients with early and untreated Graves' disease; and (iii) patients with Graves' disease studied after treatment. In 18 normal subjects and in 20 patients with treated Graves' disease CD14 mRNA was negatively correlated with Heg (P < 0.001). In 17 untreated patients with Graves' disease Heg and thyroid receptor autoantibodies were negatively correlated (P < 0.009). Incubation studies with mononuclear cells showed that the addition of a fragment of the central part of Heg (949 bases) to mononuclear cells decreased CD14 mRNA markedly to zero or nearly zero (P < 0.001). This response was not specific in the sense that siRNA and lipopolysaccharide also decreased CD14 mRNA, probably due to activation of the CD14/Toll-like receptor complex. Single-stranded RNA is likely to increase interferon production. Due to the anti-inflammatory effect Heg may also inhibit the early phase of TSH receptor autoantibody production Udgivelsesdato: 2008/11

Published
2008

129. Behandling af gastrointestinal blodning fra angiodysplasier med somatostatinanalogen octreotid

Author

Boesby, L., Kristensen, L.O., Christensen, Niels Juel, Boesby, L., Kristensen, L.O., and Christensen, Niels Juel

Abstract

Angiodysplasias account for 2-8% of GI-bleeding episodes. We describe a 75-year-old patient with a history of anaemia for 1 year before being diagnosed with multiple angiodysplasias in the GI-tract. The patient needed weekly blood transfusions until he started treatment with octreotide. After 4 months of treatment the need for transfusions had decreased dramatically and faeces was negative for blood. Treatment was switched to long-acting octreotide (Sandostatin Lar). The case illustrates the usefulness of somatostatin analogues in the treatment of bleeding GI-angiodysplasias Udgivelsesdato: 2008/3/10

Published
2008

131. Vasorelaxation in space.

Author

Norsk, Peter, Damgaard, Morten, Petersen, Lonnie Grove, Gybel, Mikkel, Pump, Bettina, Gabrielsen, Anders, Christensen, Niels Juel, Norsk, Peter, Damgaard, Morten, Petersen, Lonnie Grove, Gybel, Mikkel, Pump, Bettina, Gabrielsen, Anders, and Christensen, Niels Juel

Abstract

Udgivelsesdato: 2006-Jan, During everyday life, gravity constantly stresses the cardiovascular system in upright humans by diminishing venous return. This decreases cardiac output and induces systemic vasoconstriction to prevent blood pressure from falling. We therefore tested the hypothesis that entering weightlessness leads to a prompt increase in cardiac output and to systemic vasodilatation and that these effects persist for at least a week of weightlessness in space. Cardiac output and mean arterial pressure were measured in 8 healthy humans during acute 20-s periods of weightlessness in parabolic airplane flights and on the seventh and eighth day of weightlessness in 4 astronauts in space. The seated 1-G position acted as reference. Entering weightlessness promptly increased cardiac output by 29+/-7%, from 6.6+/-0.7 to 8.4+/-0.9 L min(-1) (mean+/-SEM; P=0.003), whereas mean arterial pressure and heart rate were unaffected. Thus, systemic vascular resistance decreased by 24+/-4% (P=0.017). After a week of weightlessness in space, cardiac output was increased by 22+/-8% from 5.1+/-0.3 to 6.1+/-0.1 L min(-1) (P=0.021), with mean arterial pressure and heart rate being unchanged so that systemic vascular resistance was decreased by 14+/-9% (P=0.047). In conclusion, entering weightlessness promptly increases cardiac output and dilates the systemic circulation. This vasorelaxation persists for at least a week into spaceflight. Thus, it is probably healthy for the human cardiovascular system to fly in space.

Published
2005

132. Hemodynamic and neuroendocrine responses to changes in sodium intake in compensated heart failure.

Author

Damgaard, Morten, Norsk, Peter, Gustafsson, Finn, Kanters, Jørgen K, Christensen, Niels Juel, Bie, Peter, Friberg, Lars, Gadsbøll, Niels, Damgaard, Morten, Norsk, Peter, Gustafsson, Finn, Kanters, Jørgen K, Christensen, Niels Juel, Bie, Peter, Friberg, Lars, and Gadsbøll, Niels

Abstract

Udgivelsesdato: 2006-May, Patients with untreated heart failure (HF) exhibit a blunted hemodynamic and neuroendocrine response to a high sodium intake, leading to excessive sodium and water retention. However, it is not known whether this is the case for patients with compensated HF receiving angiotensin-converting enzyme inhibitors and beta-adrenoreceptor blockers. Therefore, we determined the hemodynamic and neuroendocrine responses to 1 wk of a low-sodium diet (70 mmol/day) and 1 wk of a high-sodium diet (250 mmol/day) in 12 HF patients and 12 age-matched controls in a randomized, balanced fashion. During steady-state conditions, hemodynamic and neuroendocrine examinations were performed at rest and during bicycle exercise. In seated HF patients, high sodium intake increased body weight (1.6 +/- 0.4%), plasma volume (9 +/- 2%), cardiac index (14 +/- 6%), and stroke volume index (21 +/- 5%), whereas mean arterial pressure was unchanged. Therefore, the total peripheral resistance decreased by 10 +/- 4%. Similar hemodynamic changes were observed during an incremental bicycle exercise test. Plasma concentrations of angiotensin II and norepinephrine were suppressed, whereas plasma pro-B-type natriuretic peptide remained unchanged. In conclusion, high sodium intake was tolerated without any excessive sodium and water retention in medically treated patients with compensated HF. The observation that high sodium intake improves cardiac performance, induces peripheral vasodilatation, and suppresses the release of vasoconstrictor hormones does not support the advice for HF patients to restrict dietary sodium.

Published
2005

137. Effects of sodium intake on cardiovascular variables in humans during posture changes and ambulatory conditions.

Author

Damgaard, Morten, Gabrielsen, Anders, Heer, Martina, Warberg, Jørgen, Bie, Peter, Christensen, Niels Juel, Norsk, Peter, Damgaard, Morten, Gabrielsen, Anders, Heer, Martina, Warberg, Jørgen, Bie, Peter, Christensen, Niels Juel, and Norsk, Peter

Abstract

Udgivelsesdato: 2002-Dec, The hypothesis was tested that cardiac output (CO) and stroke volume (SV) are increased by a moderate physiological elevation in sodium intake with a more pronounced effect in the ambulatory upright seated than supine position. Fourteen healthy males were investigated during ambulatory and controlled laboratory conditions at the end of two consecutive 5-day periods with sodium intakes of 70 (low) and 250 (high) mmol/24 h or vice versa, respectively. Comparing high and low sodium intake, plasma volume and plasma protein concentrations were 9 and 8% higher in the seated and the supine position, respectively. When seated during laboratory conditions, CO was 5.3 +/- 0.2 l/min on the high sodium intake vs. 4.8 +/- 0.2 l/min on the low (P < 0.05), and SV was 81 +/- 3 vs. 68 +/- 3 ml (P < 0.05). In the supine position, SV was 107 +/- 3 ml on the high vs. 99 +/- 3 ml (P < 0.05) on the low sodium intake, while CO remained unchanged. The difference in CO and SV induced by the change in sodium intake was significantly higher in the seated than in the supine position (P < 0.05). During upright ambulatory conditions, CO was 5.9 +/- 0.2 l/min during the high and 5.2 +/- 0.2 l/min during the low sodium intake (P < 0.05), and SV was 84 +/- 3 and 69 +/- 3 ml (P < 0.05), respectively. Mean arterial pressure was unchanged by the variations in sodium intake. In conclusion, increments in sodium intake within the normal physiological range increase CO and SV and more so in the seated vs. the supine position. These changes are readily detectable during upright, ambulatory conditions. The results indicate that the higher SV and CO could constitute an arterial baroreflex stimulus for the augmented renal sodium excretion.

Published
2002

138. Comparison of acute cardiovascular responses to water immersion and head-down tilt in humans.

Author

Shiraishi, Makoto, Schou, Morten, Gybel, Mikkel, Christensen, Niels Juel, Norsk, Peter, Shiraishi, Makoto, Schou, Morten, Gybel, Mikkel, Christensen, Niels Juel, and Norsk, Peter

Abstract

Udgivelsesdato: 2002-Jan, The hypothesis was tested that acute water immersion to the neck (WI) compared with 6 degrees head-down tilt (HDT) induces a more pronounced distension of the heart and lower plasma levels of vasoconstrictor hormones. Ten healthy males underwent 30 min of HDT, WI, and a seated control (randomized). During WI, left atrial diameter and stroke volume increased to the same extent as during HDT. Cardiac output increased by 1 l/min more during WI than during HDT. (P < 0.05). Plasma atrial natriuretic peptide increased during WI (P < 0.05) but not during HDT, whereas plasma norepinephrine, vasopressin, and renin activity were suppressed similarly. Mean arterial pressure decreased by 9 mmHg (P < 0.05) during HDT and was unchanged during WI, and heart rate decreased more during HDT (P < 0.05). Arterial pulse pressure increased considerably more during HDT than during WI. In conclusion, the hypothesis was not confirmed because the cardiac atria were similarly distended by acute HDT and WI and the release of vasoconstrictor hormones were suppressed to the same extent.

Published
2002

149. Sympathetic Nervous Regulation in Patients with Cirrhosis: Pathogenesis of Fluid Retention and Formation of Ascites

Author

Henriksen, Jens H, Ring-Larsen, Helmer, and Christensen, Niels Juel

Subjects
Article Subject
Abstract

Increased circulating noradrenaline in patients with cirrhosis is due to enhanced sympathetic nervous activity and is not merely the result of decreased clearance of catecholamines. There is a direct relation between the level of arterial norndrenaline and severity of cirrhosis, increased portal pressure and fluid accumulation; patients with the hepatorenal syndrome exhibit the highest values of plasma noradrenaline. In patients with cirrhosis, the kidneys have been identified as an important source of noradrenaline ‘spillover’ into plasma, which indicates enhanced sympathetic nervous activity in these organs. Moreover, the level of plasma noradrenaline is inversely related to renal bloodflow and urinary excretion of sodium, and directly related to plasma renin, vasopressin and aldosterone. An increased spillover of noradrenaline has recently been demonstrated in the splanchnic system and superior portosystemic collaterals. Reduced central and arterial blood volume and low arterial blood pressure secondary to peripheral vasodilation are probably important afferent stimuli for enhanced sympathetic nervous activity, although a nonvolume-dependent hepatic baroreceptor may also be present. The authors conclude that the sympathetic nervous system, in concert with other regulatory systems, plays an important role in sodium-water homeostasis and fluid retention, as well as in the systemic and hepatosplanchnic circulatory derangement seen in patients with cirrhosis.

Published
1991
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