【Objective】 To explore the effects of apelin postconditioning on isolated rat heart ischemia reperfusion injury and investigate the underlying signal mechanism. 【Methods】 Thirty-two rats were randomized to 4 groups: ischemia reperfusion (IR) control group

IR treated with apelin postconditioning group

IR treated with apelin postconditioning and phosphatidylinositol-3-kinase (PI3K) inhibitor wortmannin group

and IR treated with wortmannin alone to evaluate the effects of apelin postconditioning on left ventricular systole pressure

coronary artery flow

creatine phosphokinase (CK) and lactate dehydrogenase (LDH) release

and the level of myocardial phospho-protein kinase B/Akt (Ser473). 【Results】 Left ventricular systole pressure

heart rate

and coronary artery flow were improved significantly

and the release of CK and LDH was reduced significantly in apelin postconditioning group as compared to ischemia reperfusion control group. Moreover

the levels of phospho-protein kinase B/Akt (Ser473) was increased in apelin postconditioning group compared with ischemia reperfusion control group. Wortmannin inhibited the increase of phospho-protein kinase B/Akt (Ser473) induced by apelin postconditioning

and abolished the cardioprotection of apelin postconditioning. 【Conclusion】 Apelin postconditioning attenuates isolated rat heart ischemia reperfusion injury. The PI3K/Akt signal pathway is involved in the cardioprotection of apelin postconditioning.