AJP - Regulatory, Integrative and Comparative Physiology, Vol 268, Issue 1 171-R182, Copyright © 1995 by American Physiological Society
Influence of nitric oxide on the hemodynamic response to hemorrhage in conscious rabbits
M. A. Koch, E. M. Hasser and J. C. Schadt
Dalton Cardiovascular Research Center, Department of Veterinary Biomedical Sciences, University of Missouri, Columbia 65211.
We investigated the role of nitric oxide, an endothelium-derived relaxing
factor, in the hemodynamic response to acute hemorrhage in conscious
rabbits. Chronically instrumented rabbits were treated with the nitric
oxide synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) or
vehicle and hemorrhaged until mean arterial pressure fell below 40 mmHg.
Control animals were treated with L-NAME or vehicle but not subjected to
hemorrhage. L-NAME increased mean arterial pressure and decreased heart
rate in control animals. Hindquarters and mesenteric blood flow velocity
and conductance were reduced by L-NAME. Nitric oxide synthase inhibition
also produced significant changes in the hemodynamic response to
hypotensive hemorrhage. Mean arterial pressure was higher and regional
vascular conductances were lower throughout hemorrhage and during recovery.
L-NAME treatment significantly (but in some cases, subtly) altered the
characteristic pattern of changes in vascular conductance associated with
acute hypotensive hemorrhage and recovery. Similar experiments with other
arginine analogues or phenylephrine infusion showed that L-NAME's effects
during hemorrhage were due to nitric oxide synthase inhibition. We conclude
that nitric oxide plays a role in the hemodynamic response to acute
hemorrhage in the rabbit and is essential for the full expression of the
vasodilation associated with hypotensive hemorrhage.
