Isoflurane-induced postconditioning via mitochondrial calcium-activated potassium channels

Purpose : Activation of the mitochondrial calcium-activated potassium (mKCa) channel reportedly confers resistance to myocardial ischemic stress. However, the role of the mKCa channel in postconditioning induced by volatile anesthetic remains unclear. Methods : Male Japanese white rabbits underwent coronary artery occlusion for 30 min followed by reperfusion for 3 h. Volatile anesthetic, isoflurane, was administered at 3 min prior to reperfusion for 5 min. Rabbits were injected with the mKCa channel blocker, iberiotoxin, or the mKCa channel opener, NS1619, at 8 min prior to reperfusion. Myocardial infarct size and the area at risk (AAR) were measured at the end of the experiment. Results : Isoflurane significantly reduced infarct size (23.0 9.8% f the AAR, P 0.05) compared with the control (44.0 9.1% Iberiotoxin abolished the cardioprotective impact of isoflu- rane (43.0 11.6% while iberiotoxin alone exerted no effect on infarct size (45.0 9.5% NS1619 and isoflurane/ NS1619 both significantly reduced infarct size (21.0 10.3% nd 19.0 8.8% respectively, P 0.05 vs control group), but isoflurane/NS1619 showed no additional benefits compared with isoflurane alone. Conclusion : These results indicate that activation of the mKCa channel contribute isoflurane-induced postconditioning. J. Med. Invest. 63 : 80-84, February, 2016