In experimental models, several volatile anesthetics have been found to beneficially mimic ischemic preconditioning (IPC) during ischemia and reperfusion. These effects of IPC and volatile anesthetics are mediated by K_ATP channels, the authors examined following hypothesis: Desflurane administration before myocardial ischemia, has pharmacologic preconditioning effects on the myocardium (better functional recovory, and reduced infarct size), and these effects are mediated by K_ATP channel activation.

Isolated Sprague-Dawley rat hearts (n = 40) were perfused at a constant pressure with oxygenated modified Kreb's solution. After a stabilization period, they were subdivided into four groups; group 1 to 4. Group 1 underwent 30 minutes of global ischemia and 60 minutes of reperfusion. Group 2 received an ischemic preconditioning period before global ischemia and reperfusion as group 1. In group 3, 6.8 vol% desflurane was added to the perfusion medium for 15 minutes and a 5 minutes wash-out period was introduced before global ischemia and reperfusion. In group 4, during the 6.8 vol% desflurane administration, glibenclamide was injected at a constant rate, before global ischemia and reperfusion. In each group, isovolumetric left ventricular pressure (LVP), heart rate and the maximun rate of change of the ventricular pressure (dP/dt_max) were measured using a thin, saline-filled latex balloon and a transducer. Coronary flow and the LDH level of effluent were measured at 5, 30, 60 minutes after reperfusion. All hearts were stained with triphenyl tetrazolium to determine infarct size.

Desflurane administration before global ischemia showed protective effects, like IPC, on functional recovery and infarct reduction. LVP was less depressed in group 3 and group 2. dP/dt_max in group 2 recovered after global ischemia to some degree, but remained slightly depressed in group 3. Decreased heart rate and coronary flow were observed in groups 2, 3 and 4. LDH showed a decreasing pattern in group 2 and 3. Infarct size was smaller in groups 2 and 3 than in groups 1 and 4. These benefical effects of desflurane were blocked by glibenclamide administration.

Desflurane was found to have beneficial effects, and mimicked IPC by preservaing LVP, reducing infarct size, and the degree of cardiac enzyme release. These beneficial effects were abolished by administering the K_ATP channel blocker, glibenclamide. The protecitve effects of desflurane administration against myocardial ischemia were mediated by K_ATP channels.