Stroke, Vol 15, 690-694, Copyright © 1984 by American Heart Association
MT Bedran de Castro, GJ Crystal, HF Downey and FA Bashour
We compared vasoactive effects of intravenous nicotine (36
micrograms/kg/min) in regional cerebral circulations under pentobarbital
and chloralose anesthesia. Experiments were conducted in three groups of
dogs: Group I, pentobarbital anesthesia with fixed ventilation; Group II,
chloralose anesthesia with fixed ventilation; Group III, chloralose
anesthesia with free breathing. Values for regional cerebral blood flow
measured with 15 mu radioactive microspheres were used to compute regional
cerebral vascular resistance (rCBR). In Group I, nicotine had no effect on
rCVR in cerebral cortex, and it increased significantly rCVR in cerebellum
(+17%), pons (+13%), medulla (+23%), and spinal cord (+19%). Using
chloralose instead of pentobarbital in dogs with fixed ventilation (Group
II), caused a significant reduction in rCVR in the cerebral cortex during
nicotine, although it did not alter significantly nicotine-induced changes
in rCVR in other regions of the brain. Hypocapnic alkalosis during
nicotine-induced hyperventilation (Group III) resulted in significant
increases in rCVR in all regions of the brain; however, the increases in
rCVR in non-cortical regions more than doubled those in the cerebral
cortex. The present results indicate: Nicotine-induced vasodilation in
cerebral cortex was blunted by pentobarbital anesthesia. Nicotine- induced
vasodilation in cerebral cortex under chloralose anesthesia was sufficient
to nullify in part the potent vasoconstrictor effect of hypocapnic
alkalosis.
ARTICLES
Regional blood flow in canine brain during nicotine infusion: pentobarbital vs. chloralose anesthesia
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