Role of an ATP-Sensitive Potassium Channel Opener, YM934, in Mitochondrial Energy Production in

We examined a possible mechanism of action of an ATP-sensitive potassium (KATP) channel opener, YM934, for the improvement of energy metabolism in hearts subjected to 35-min ischemia and 60-min reperfusion. The treatment with 30 nM YM934 for the final 15 min of preischemia enhanced post-ischemic recovery of left ventricular developed pressure, atten-uated the postischemic rise in left ventricular end-diastolic pressure, and suppressed the release of creatine kinase and ATP metabolites during reperfusion. The treatment also re-stored myocardial ATP and creatine phosphate contents and attenuated the decrease in mitochondrial oxygen consumption rate during reperfusion. The higher mitochondrial function was also seen in YM934-treated hearts at the end of ischemia. In another set of experiments, myocardial skinned bundles wer