Endothelium-dependent pulmonary vasodilation in conscious dogs is selectively attenuated during isoflurane anesthesia. Gambone, Linda M., Yoshihiro Fujiwara, and Paul A. Murray. The Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins Medical Institutions, Baltimore, Maryland, Center for Anesthesiology Research, Division of Anesthesiology and Critical Care Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio
APStracts 3:0264H, 1996.
We have recently reported that halothane (HAL) anesthesia attenuates the pulmonary vasodilator responses to both bradykinin (BK) and sodium nitroprusside (SNP) compared to responses measured in the conscious state. These agonists have been classically used to activate endothelium-dependent and -independent vasodilator pathways, respectively. Our present goal was to assess the effect of isoflurane (ISO) anesthesia on pulmonary vasodilation activated via these pathways. Left pulmonary vascular pressure-flow (LPQ) plots were used to measure the pulmonary vascular responses to cumulative intravenous doses of BK, SNP and SIN-1, a nitric oxide donor, in chronically -instrumented dogs in the conscious state and during ISO anesthesia following matched preconstriction with the thromboxane analogue, U46619. ISO attenuated (p?&LT?0.05) the vasodilator response to BK. However, ISO had a differential effect on the responses to SIN-1 and SNP. ISO potentiated (p &LT 0.05) the vasodilator response to SIN-1, whereas ISO attenuated (p &LT 0.05) the response to SNP. The vasodilator response to SIN-1 was unchanged during HAL. The ATP -sensitive potassium (K+ATP) channel inhibitor, glybenclamide, attenuated (p &LT 0.05) the vasodilator response to SNP but not SIN-1. Thus, ISO and HAL selectively attenuate the endothelium -dependent pulmonary vasodilator response to bradykinin. Both anesthetics attenuate vasodilation induced by SNP, but not SIN-1. Moreover, a component of SNP-induced vasodilation involves K+ATP channel activation. 

Received 24 July 1995; accepted in final form 10 June 1996.
APS Manuscript Number H697-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 July 96