Effects Of Sevoflurane Postconditioning On Hexokinase Ⅱ In Myocardial Ischemia-reperfusion Injury In Mice

Objective: To investigate the effect of sevoflurane postconditioning on hexokinase throughout ischemia reperfusion injury.Methods: The adult male C57BL/6 mouses were randomly divided into 3 groups: sham group,ischemia reperfusion injury group(IRI)and sevoflurane postconditioning group(SPostC).Rate-pressure product(RPP)was recorded.Infarct size was mesured with TTC staining.The ultrastructure of mitochondrion and mitochondrial Hexokinase activity was observed,its concentration was also tested with western blotting,and the degree of mPTP opening was also measured as well.TUNEL method was used to detect the apoptosis of cardiomyocytes.Results: Compared with sham group,the RPP and the activity of mitochondrial HK were lower(P<0.05)and the mPTP opening level was much higher(P<0.05)after 30 minutes ischemia.Compared with IRI group,SPostC group had a higher RPP level(33650.0±5095.4bpm·mmHg vs 40444.3±4985.4bpm·mmHg,P < 0.05),lower rate of infarct size(44.6±4.7% vs 36.8±1.5%,P<0.05),Flameng grade of mitochondrion(3.6±0.3 vs 2.3±0.5,P<0.05),myocardial apoptosis(38.7±3.0% vs 31.6±2.2%,P<0.05)and level of mPTP opening(0.85±0.02 vs 0.82±0.02,P<0.05),but the mitochondrial HK activity(26.3±2.3% vs 31.3±2.9%,P<0.05)and content(0.21±0.04 vs0.30±0.03,P<0.05)were elevated by SPostC.Conclusion: Sevoflurane postconditioning could exert cardioprotection by inhibiting mPTP from persistent opening after the ischemia reperfusion injury to cardiomyocytes.This effect was achieved likely by up regulating mitochondrial HK activity.