| Objective:To investigate the effect of sevoflurane postconditioning on HIF-1α nuclear translocation during myocardial ischemia—reperfusion(I/R).Methods :forty adult male C57 mice,weighing 20—30 g,were randomized to 4 groups(n =10 each)using a random number table : sham operation group.(group Sham),I / R group,sevoflurane postconditioning group(group SPC)and inhibitor group(group 2Me2).In group sham,only thoracotomy was performed without ligation of the coronary artery.In I/R,SPC and2Me2 groups,hearts from adult male C57 mice were exposed and subjected to 30 min of ischemia and 120 min of reperfusion.In group SPC 2.4% sevoflurane was inhaled for 15 min starting from the onset of reperfusion to perform sevoflurane postconditioning.In group 2Me2,2Me2 was injected 30 min before anesthetized(intraperitoneal).At 120 min of reperfusion,the mice were put to death,and remove the hearts.Measure heart rate(HR),systolic pressure(SBP),mean arterital pressure(MAP),myocardial infarct size.HIF-1αexpression in cytoplasm and nucleus respectively(by western blot).Results: Compared with group sham,myocardial infarct size,SBP,MAP decrease in group I/R and 2Me2,HIF-1αnuclear translocation increased in group I / R,HIF-1α nuclear translocation decrease in group 2Me2(P<0.05);myocardial infarct size remarkably decreased,HIF-1αnuclear translocation significantly increased in group SPC(P<0.05).Compared with group I/R,myocardial infarct size remarkably decreased,HIF-1α nuclear translocation significantly increased in group SPC;myocardial infarct size increased,SBP,MAP,HIF-1α nuclear translocation decreased and in group 2Me2(P<0.05).Compared with group SPC,myocardial infarct size,HR increased and SBP,MAP,HIF-1α nuclear translocation decreased in group 2Me2(P<0.05).Conclusion:The mechanism by whichsevoflurane postconditioning reduced myocardial ischemical reperfusion injury is related to raise HIF-1α nuclear translocation. |