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Muscle chemoreflex-induced increases in right atrial pressure
Flight Motion Effects Branch, Air Force Research Laboratory, Brooks Air Force Base, San Antonio, Texas 78235; and Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201 When oxygen delivery to active muscle is too low for the ongoing rate of metabolism, metaboli...
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Published in: | American journal of physiology. Heart and circulatory physiology 1998-09, Vol.275 (3), p.H767-H775 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Flight Motion Effects Branch, Air Force Research Laboratory, Brooks
Air Force Base, San Antonio, Texas 78235; and Department of
Physiology, Wayne State University School of Medicine, Detroit,
Michigan 48201
When oxygen delivery to active muscle is too low
for the ongoing rate of metabolism, metabolites accumulate and
stimulate sensory nerves within the muscle leading to sympathetic
activation (muscle chemoreflex). To date, studies on this reflex have
focused primarily on its ability to increase arterial pressure or on
the activity of the nerves that mediate this response. Clearly, a rise
in cardiac output (CO) constitutes an important adjustment, because it
increases the total blood flow available to be distributed among organs
competing for flow. However, increments in heart rate and contractility
provide limited means of raising CO because of the inverse relationship
that exists between CO and right atrial pressure (RAP) in the intact
circulation. Our goal was to test whether muscle chemoreflex
activation, achieved via graded reductions in hindlimb blood flow by
partial vascular occlusion, elicits peripheral vascular adjustments
that raise RAP. In four conscious dogs exercising on a treadmill at 3.2 km/h 0% grade, RAP was well maintained during reflex activation
despite increases in CO and arterial pressure that are expected to
reduce RAP. Thus peripheral vascular adjustments elicited by the reflex
successfully defend RAP in a setting where it would otherwise fall. To
isolate the effects of the reflex on RAP, CO was maintained constant by
ventricular pacing in conjunction with
1 -adrenergic blockade with
atenolol. When the reflex was activated by reducing hindlimb blood flow from 0.6 to 0.3 l/min, RAP rose from 5.1 ± 0.8 to 7.4 ± 0.4 mmHg ( P |
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ISSN: | 0363-6135 1522-1539 |
DOI: | 10.1152/ajpheart.1998.275.3.h767 |