2016 Volume 63 Issue 1.2 Pages 80-84
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% of the AAR, P<0.05) compared with the control (44.0±9.1%). Iberiotoxin abolished the cardioprotective impact of isoflurane (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% and 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
