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1 Danish Aerospace Medical Centre of Research and 2 The Heart Center, National University Hospital, Rigshospitalet, DK-2100 Copenhagen; 3 Department of Medical Physiology, Panum Institute, University of Copenhagen, DK-2200 Copenhagen; and 4 Department of Internal Medicine and Endocrinology, Herlev Hospital, University of Copenhagen, DK-2730 Herlev, Denmark
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 ± 0.02 (SE)] and 10 age-matched controls (ejection fraction = 0.68 ± 0.03) underwent 30 min of thermoneutral (34.7 ± 0.02°C) water immersion (WI) to the xiphoid process. WI increased
(P < 0.05) central venous pressure by 3.7 ± 0.6 and 3.2 ± 0.4 mmHg and stroke volume index by 12.2 ± 2.1 and 7.2 ± 2.1 ml · beat
1 · m
2 in controls
and HF patients, respectively. During WI, systemic vascular resistance
decreased (P < 0.05) similarly by 365 ± 66 and
582 ± 227 dyn · s · cm
5 in controls
and HF patients, respectively. Forearm subcutaneous vascular resistance
decreased by 19 ± 7% (P < 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; renin-angiotensin system; endothelin; baroreceptors
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