Cardioprotective effect of ischemic postconditioning and its relationship to the mitochondrial permeability transition pore

Aim. The purpose of the present study was to investigate cardioprotection and possible ischemic postconditioning (IPO) during myocardial ischemia-reperfusion injury. Methods. We established an acute myocardial ischemia-reperfusion model where the left anterior descending coronary artery (LAD) was ligated for 30 min and reperfused for 60 min in vivo. Thirty-two healthy male SD rats were randomly divided into the sham-operated group, the ischemia-reperfusion group (IR), the IPO group and the group receiving the mitochondrial permeability transition pore inhibitor cyclosporine A (CsA). IPO was achieved by three cycles of pre-reperfusion for 30 seconds followed by a persistent reperfusion for 60 min. CsA was administered before reperfusion. The activities of creatine kinase (CK) and superoxide dismutase (SOD) and the concentration of malondialdehyde (MDA) were also measured. The mitochondrial morphologies and ultrastructural parameters in the experimental groups were observed by electron microscopy. Moreover, Cytochrome C and caspase-3 expression was measured by immunohistochemistry. Results. Compared with the IR group, the concentration of MDA and the activity of CK were significantly attenuated in the IPO group (P<0.01), whereas the activity of SOD was markedly enhanced (P<0.01). Cyt C and caspase-3 expression and mitochondrial ultrastructural damage were also clearly reduced. Moreover, the IPO group exhibited myocardial protection similar to the mPTP inhibitor CsA. Conclusion. IPO had an effect on myocardical protection that was similar to the effect of mPTP inhibitor CsA on the reduction of apoptosis induced by ischemia-reperfusion injury.