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AJP - Heart and Circulatory Physiology, Vol 259, Issue 4 1197-H1206, Copyright © 1990 by American Physiological Society
ARTICLES |
L. B. Rowell and D. R. Seals
Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle 98195.
To determine how hypoxemia (Hx) might alter muscle sympathetic nerve activity (MSNA) (microneurography, peroneal nerve), norepinephrine (NE) levels, and vasoconstriction during mild central hypovolemia, we exposed eight men to continuous graded lower body negative pressure (LBNP) (-5, -10, -15, -20, and -25 mmHg, 5 min per level) during both Hx (10 or 12% O2) and normoxia (Nx). Hx significantly augmented MSNA during LBNP. Total MSNA (average amplitude X burst frequency) rose at each level of LBNP by 2, 28, 93, 61, and 123% (Nx) and 32, 110, 127, 179, and 216% (Hx). Only at LBNP -20 and -25 mmHg did Hx significantly augment the increase in forearm venous NE concentration. Arterial pressure was unaffected by LBNP in Nx and Hx. Forearm blood flow (venous occlusion plethysmography) fell, and forearm vascular resistance (FVR) rose 23, 53, 65, 67, and 86% (Nx) vs. 22, 23, 60, 69, and 87% (Hx), but increments in FVR (absolute units) were significantly less in Hx. Correlations among MSNA and other variables were insignificant for pooled data owing to large inter-individual variations in slopes, but correlations were significant for total MSNA (and burst frequency) vs. FVR (Nx) and NE (Hx). Three men released epinephrine during LBNP; this was accompanied by forearm vasodilation and falling pressure, and in two men, decreased MSNA and bradycardia occurred (i.e., vasovagal reaction). Overall, we found no major defect in sympathetic control during graded hypovolemia and Hx as long as epinephrine levels did not rise.
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