The Role of Mitochondrial KATP Channels in the Infarct-Reducing Effect of Normobaric Hypoxia

We studied the role of K ATP channels in the infarct-limiting effect of short-term normobaric hypoxia. Male Wistar rats were subjected to a 45-min coronary artery occlusion followed by a 120-min reperfusion. Normobaric hypoxia was simulated 30 min before coronary artery occlusion: 6 sessions of hypoxia (8% O 2 , 10 min) and reoxygenation (21% O 2 , 10 min). The following drugs were administered to rats: glibenclamide, 5-hydroxydecanoate, and HMR1098. It was found that normobaric hypoxia contributes to a decrease in myocardial infarct size by 36%. Preliminary administration of glibenclamide or 5-hydroxydecanoate eliminated the infarct-reducing effect of normobaric hypoxia. Activator of mitochondrial K ATP channel diazoxide limited the infarct size. These findings suggest that mitochondrial K ATP channels are involved into the cardioprotective effect of normobaric hypoxia