AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 261: H1903-H1912, 1991;
0363-6135/91 $5.00
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AJP - Heart and Circulatory Physiology, Vol 261, Issue 6 1903-H1912, Copyright © 1991 by American Physiological Society

ARTICLES

Carotid baroreceptor control of right atrial mechanics in dogs

D. E. Carlson, M. J. Brunner and D. S. Gann
Department of Surgery, University of Maryland School of Medicine, Baltimore 21201.

To investigate the influence of the carotid arterial baroreceptors on right atrial mechanics, the carotid sinus region was isolated surgically in eight dogs prepared acutely under pentobarbital. Right atrial pressure and conductance volume were measured with a strain-gauge tip catheter and a conductance catheter, respectively. Reduction of carotid sinus pressure from 225 to 50 mmHg elicited significant increases in the a wave in right atrial pressure, in atrial stroke volume, in atrial stroke work (2.5-fold), and in atrial stroke power (4-fold). Mean central venous pressure and atrial volume at the onset of each beat did not change. These responses were unchanged after bilateral cervical vagotomy. Head-up tilt was applied at carotid sinus pressures less than or equal to 150 mmHg in four dogs to oppose any contribution of decreased systemic venous capacity to the responses through increased atrial filling. Tilt did not change atrial stroke work or atrial filling during late ventricular systole before vagotomy but inhibited these variables significantly after vagotomy. The slope of the relationship between right atrial stroke work and atrial volume at the onset of contraction increased significantly with reduction of carotid sinus pressure. This response was unaffected by either vagotomy or tilt. Carotid arterial hypotension appears to augment right atrial stroke work and stroke volume through an increase in atrial contractility. A decrease in venous capacity may contribute to this response especially after vagotomy.


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S. S. Blevins, M. J. Connolly, and D. E. Carlson
Baroreceptor-mediated compensation for hemodynamic effects of positive end-expiratory pressure
J Appl Physiol, January 1, 1999; 86(1): 285 - 293.
[Abstract] [Full Text] [PDF]


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