Medullary vasomotor activity and hypoxic sympathoexcitation in
pentobarbital-anesthetized rats.
Sun, Miao-Kun, and Donald J. Reis.
Department of Neurology and Neuroscience, Cornell University
Medical College, 411 East 69th Street, New York, NY 10021 USA
APStracts 2:0251R, 1995.
In sodium pentobarbital-anesthetized, paralyzed, and ventilated rats,
systemic hypoxia, produced by intratracheal N2 administration for 20
s, rapidly increased activities of reticulospinal vasomotor neurons
in the rostroventolateral reticular nucleus (RVL) of the medulla
oblongata (by 23.9+/-4.7 spikes/s) and sympathetic nerves (by 30.9+/
-4.7 _V) and arterial pressure (by 35.6+/-6.4 mmHg). The
sympathoexcitatory and pressor responses were abolished by bilateral
microinjections of muscimol, a GABAA receptor agonist, (250
pmol/50nl/site) into RVL. Chemical inhibition of RVL also reduced
arterial pressure to 48.1+/-3.7 mmHg and eliminated sympathetic nerve
activity. Intravenous infusion of L-phenylephrine and intrathecal
administration of kainic acid restored arterial pressure to control
level but not the rapid sympathoexcitatory responses to acute
hypoxia. We conclude that in pentobarbital-anesthetized rats, the
sympathetic vasomotor tone and pressor responses to acute hypoxia
depend on activity and excitation of RVL-spinal vasomotor neurons.
The neural mechanisms responsible for the sympathetic tone and rapid
pressor responses to hypoxia in these animals do neither
qualitatively differ from those anesthetized with urethane nor from
the decerebrate unanesthetized animals.
Received 1 May 1995; accepted in final form 27 August 1995.
APS Manuscript Number R259-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 September 1995.