BLOCKADE OF ATP-SENSITIVE K+ CHANNEL ABOLISHES THE ANTIISCHEMIC EFFECTS OF ISOFLURANE IN DOG HEARTS

Background: Although isoflurane is reported to have a protective effec t against ischemic damage on the myocardium, the mechanisms of this ef fect are not clear. Activation of adenosine triphosphate sensitive pot assium (KATP) channels is indicated to protect myocardium during ische mia. Thus, it was hypothesized that if isoflurane could activate KATP channels, blockade of KATP channels would decrease its cardioprotectiv e effect. Methods: Mongrel dogs, anesthetized with morphine, urethane, and chloralose, were subjected to 15 min of left anterior descending coronary artery occlusion followed by 60 min reperfusion. The dogs wer e divided into three groups: the control group (n=8), ISO group (n=8) and ISOGC group (n=8). In the ISO and ISOGC groups, 1 MAC of isofluran e was administrated during ischemia and reperfusion. In the ISOGC grou p, 0.3 mg/ kg of glibenclamide, the KATP channel blocker, was given 45 min before ischemia. Full-thickness samples of myocardium were obtain ed and the concentrations of adenosine monophosphate, adenosine diphos phate, adenosine triphosphate (ATP), creatine phosphate and lactate in the endocardial portion of the myocardium were measured. Results: The ischemia-reperfusion caused a 25.4% and 27.6% reduction of myocardial ATP in the control and ISOGC groups, respectively. In contrast, the I SO group showed only 11.0% reduction of ATP, which was significantly l ower compared to the other groups (P<0.01). Conclusions: Our results s hows that blockade of the KATP channel abolishes cardioprotective effe cts of isoflurane in myocardial ischemia-reperfusion. The KATP channel may play a role in the ATP-sparing effect of isoflurane. (C) Acta Ana esthesiologica Scandinavica 41 (1997).