Loading…

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...

Full description

Saved in:
Bibliographic Details
Published in:American journal of physiology. Heart and circulatory physiology 1998-09, Vol.275 (3), p.H767-H775
Main Authors: Sheriff, Don D, Augustyniak, Robert A, O'Leary, Donal S
Format: Article
Language:English
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
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  
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.1998.275.3.h767