Abstract: Abstract： Objective To observe the postconditioning cardioprotective effects of atorvastatin (ATV) on ischemia-re⁃ perfusion injury in isolated rat heart, and the role of phosphatidylinositol-3-kinase , protein kinase B(PI3K-Akt), mitochon⁃ drial ATP-sensitive potassium (mito-KATP channel) and mitochondrial permeability transition pore (mPTP) thereof. Meth⁃ ods Healthy male Wistar rats were randomly divided into 9 groups: ischemia reperfusion (I/R) control group, atorvastatin postconditioning (ATV) group, ATV plus PI3K inhibitor LY294002 (ATV+LY294002) group, LY294002 group, ATV plus mi⁃ to-KATP channel inhibitor 5-hydroxydecanoate (ATV+5-HD) group, 5-HD group, ATV plus mPTP inhibitor ATR (ATV+ ATR) group, ATR group and ethanol group. Model rats were given 30-min ischemia followed by 120-min reperfusion. The myocardial infarction size, hemodynamic parameters, creatine kinase isoenzyme (CK-MB), lactate dehydrogenase (LDH), nic⁃ otinamide adenine dinucleotide (NAD+) and the expression of myocardial protein kinase B (Akt) and myocardial phospho-pro⁃ tein kinase B (p-Akt) were evaluated. Results Compared with the control group, atorvastatin reduced the myocardial in⁃ farction size, CK-MB and LDH（P＜ 0.05), increased NAD（ + P＜ 0.05). There were no significant differences in the myocardi⁃ al infarction size, CK-MB, LDH and NAD + between ATV+LY294002 group, ATV+5-HD group and ATV+ATR group. The hemodynamic parameters were improved in ATV group compared with those in control group. Western blot analysis con⁃firmed the significant phosphorylation of Akt in ATV group, ATV+5-HD group and ATV+ ATR group compared with those of control group. There were no significant differences in the phosphorylation of Akt between ATV + LY294002 group, LY294002 group, ATR group and 5-HD group. Conclusion Atorvastatin postconditioning could attenuate the ischemia-re⁃ perfusion injury through activating the PI3K-Akt, promoting mito-KATPchannel opening and inhibiting mPTP opening.

Key words: myocardial reperfusion injury, 1-phosphatidylinositol 3-kinase, KATP channels, adenosine triphosphate, mitochondria, cell membrane permeability, atorvastatin postconditioning