Effects of Isoflurane Anesthesia on Pulmonary Vascular Response to K (ATP)+ Channel Activation and Circulatory Hypotension in Chronically Instrumented Dogs

Background: The objective of this study was to evaluate the effects of isoflurane anesthesia on the pulmonary vascular responses to exogenous adenosine triphosphate-sensitive potassium (KATP+) channel activation and circulatory hypotension compared with responses measured in the conscious state. In addition, the extent to which KATP+ channel inhibition modulates the pulmonary vascular response to circulatory hypotension in conscious and isoflurane-anesthetized dogs was assessed.

Methods: Fifteen conditioned, male mongrel dogs were fitted with instruments for long-term monitoring to measure the left pulmonary vascular pressure-flow relation. The dose-response relation to the KATP+ channel agonist, lemakalim, and the pulmonary vascular response to circulatory hypotension were assessed in conscious and isoflurane-anesthetized (approximately 1.2 minimum alveolar concentration) dogs. The effect of the selective KATP+ channel antagonist, glibenclamide, on the pulmonary vascular response to hypotension was also assessed in conscious and isoflurane-anesthetized dogs.

Results: Isoflurane had no effect on the baseline pulmonary circulation, but it attenuated (P < 0.05) the pulmonary vasodilator response to lemakalim. Reducing the mean systemic arterial pressure to approximately 50 mmHg resulted in pulmonary vasoconstriction (P < 0.05) in the conscious state, and this response was attenuated (P < 0.05) during isoflurane. Glibenclamide had no effect on the baseline pulmonary circulation, but it potentiated (P < 0.05) the pulmonary vasoconstrictor response to hypotension in conscious and isoflurane-anesthetized dogs.