[The role of sarcolemmal and mitochondrial K(ATP)-channels in realization of the cardioprotection and antiarrhythmic effect of different regimens of hypobaric adaptation].

The aim of study was an investigation of the role of different types of K(ATP)-channels in the increased tolerance to the rat heart to ischemic and reperfusion arrhythmias after the different regimes ofhypoxic adaptation. Wistar rats were exposed to an intermittent hypoxia in two different regimens: 5000 m, 6 h/day during 6 weeks or 7000 m, 8 h/day during 7 weeks. It has been found that both types of adaptation increase cardiac tolerance to arrhythmogenic impact of acute ischemia, but only training at 7000 m induces cardioprotective effect. Inhibition of mitK(ATP)-channels by pretreatment with 5-hydroxydecanoate (5 mg/kg) or MCC-134 (3 mg/kg) completely abolishes cardioprotection and antiarrhythmic effect of adaptation in the 7000 m regimen. Antiarrhythmic effect of adaptation in the 5000 m regimen is eliminated by injection of glibenclamide (0.3 mg/kg), an inhibitor of sarcolemmal and mitochondrial K(ATP)-channels. It has been proposed that in cardioprotection of adaptation in the 7000 m regimen mitK(ATP)-channels play a considerable role, whereas in the 5000 m regimen sarcK(ATP)-channels are involved. Antiarrhythmic effect and cardioprotectio has not been found during experiments on the isolated perfused rat heart.