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Objective To evaluate the role of 1-phosphatidlylinositol 3-kinase/protein-serine-threonine kinase(PI3K/Akt)and mitochondrial permeability transition pore(mPTP)in alleviating cardiomyocyte apoptosis induced by sufentanil postconditioning during myocardial ischemia-reperfusion in rats.Methods Twenty-four healthy male SD rats weighing 250-300g were randomly divided into 4 groups(n = 6 each): sham operation group(group S); ischemia-reperfusion group(group IR); sufentanil postconditioning group(group SP)and sufentanil postconditioning+Wortmannin group(group SP+W).The model of myocardial IR was induced by temporary ligation to the anterior descending branch of left coronary artery maintained for 30 min,followed by 120 min reperfusion.Group S only thread ligation,Group SP and SP+W received sufentanil 1.0 μg/kg at 5 min before reperfusion,while group SP+W received wortmannin 15ug/kg before sufentanil injection.After 120 min of reperfusion,draw blood from aorta abdominalis and determin the concentration of troponin(cTnI)and creatine kinase isoenzyme(CK-MB)in serum.Then the hearts were immediately removed for calculation of myocardial apoptosis index(AI)by TUNEL,measurement of myocardial NAD+content by spectrophotometry at 440 nm and determination to expression of Akt and phosphorylated Akt(p-Akt)by Western blotting.After the separation of the mitochondria and cytoplasm,detect the expression levels of cytochrome-C(Cyt-C)and apoptosis inducing factor(AIF)individually by Western blotting too.Results Compared with group S,cardiomyocyte apoptosis increased,NAD+content decreased,the expression of CytC and AIF down in mitochondria,while up in cytoplasm and p-Akt up in group IR,SP and SP+W(P<0.05).Compared with group IR,cardiomyocyte apoptosis decreased,NAD+content increased,the expression of CytC and AIF up in mitochondrial,while down in cytoplasm and p-Akt up in group SP(P<0.05).Conclusion Sufentanil postconditioning may attenuate cardiomyocyte apoptosis by IR injury in rat hearts through activating PI3K/Akt and inhibiting mPTP opening.