AJP - Regulatory, Integrative and Comparative Physiology, Vol 260, Issue 4 739-R746, Copyright © 1991 by American Physiological Society
Sympathoadrenal activation in sinoaortic-denervated rats following endotoxin
Z. Z. Zhou, R. D. Wurster, M. Qi and S. B. Jones
Department of Physiology, Stritch School of Medicine, Loyola University of Chicago, Maywood, Illinois 60153.
We evaluated the role of the baroreceptor reflex in mediating the
sympathoadrenal activation during endotoxicosis, using acutely as well as
chronically denervated rats. Three groups of experiments were conducted. In
the first experiment, hemodynamic and plasma catecholamine responses
following endotoxin (5 mg/kg iv) were measured in
alpha-chloralose-anesthetized rats with acute sinoaortic baroreceptor
denervation (SAD) or sham operation. In the second experiment, chronically
sinoaortic-denervated rats and sham controls were used and experiments were
conducted as in acute preparations. In the third experiment hydralazine (1
mg/kg iv) was given to chronically denervated rats and sham controls to
evaluate the singular contribution of hypotension-evoked baroreflex
disinhibition in the absence of endotoxin. In both acute and chronic
preparations, endotoxin induced marked elevation of plasma norepinephrine
and epinephrine in the presence as well as the absence of arterial
baroreceptors (P greater than 0.05). Plasma catecholamines were
significantly increased by hydralazine-induced hypotension in the sham
group, but this elevation was far less than that induced by endotoxin.
Hypotension alone did not significantly increase plasma catecholamines in
SAD rats. These results suggest that the baroreflex is not the major factor
in mediating sympathoadrenal activation during endotoxicosis and that
non-baroreflex mechanisms may be involved in stimulating such activation.
