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.