Abstract:Aim To investigate the effects of minocycline postconditioning on myocardial ischemia-reperfusion injury in rats and its possible mechanism. Methods Ninety-six male Wistar rats were randomly divided into four groups：sham-operation group，ischemia-reperfusion（IR） group，low-dose minocycline （3 mg/kg） group and high-dose minocycline （10 mg/kg） group. The rat model of myocardial IR was established by occlusion of the left anterior descending coronary artery for 45 min and reperfusion for 2 hours or 24 hours. After 2 h reperfusion,myocardial area at risk and infarct size were evaluated the amount of TNF-α,IL-1β in serum and myocardium and cardiac MPO activity were assayed myocardial apoptosis index（AI） and the myocardial tissue morphology were detected. The parameters of haemodynamics and myocardial area at risk and infarct size were evaluated 24 h after reperfusion. Results Compared with IR group,both low-dose and high-dose minocycline reduced LVEDP,enhanced HR,LVSP and±dp/dtmax,lowered the amount of TNF-α,IL-1β in serum and myocardium,cardiac MPO activity,and AI （P<0.05 or P<0.01）. Conclusion Minocycline postconditioning may ameliorate heart functions and decrease the infarct size and myocardial apoptosis induced by myocardial IR injury in vivo rats,and the protective effect may be related to interfering with the local and systemic inflammatory reactions.

Abstract:Aim To study the effect and possible mechanism of nicorandil postconditioning on myocardial ischemia reperfusion(MIR) injury in rats. Methods The SD rats were randomly divided into six groups: control group,ischemia reperfusion group,postconditioning group,nicorandil postconditioning groups of 2 mg/kg,5 mg/kg,and 10 mg/kg.Ischemia reperfusion group was obtained by ligated left anterior descending coronary artery 30 minutes and followed by 120 minutes reperfusion.Postconditioning group was obtained by 5 cycles of brief 10 seconds intermittent reperfusion/reocclusion.After 30 minutes ischemia,hearts were exposed to nicorandil for 10 minutes immediately at the onset of reperfusion.Contents of creatine kinase(CK) and malondialdehyde(MDA),activity of superoxide dismutase(SOD) were detected respectively.Apoptosis rates and the expression of caspase-3 were investigated. Results In the nicorandil postconditioning groups,contents of CK and MDA were lower,activities of SOD were higher,apotosis rates were decreased,and caspase-3 was lower. Conclusions Nicorandil postconditioning could protect MIR.The myocardial protective mechanism maybe realized by enhancing the activity of SOD,enhancing myocardial antioxygen capability,reducing the oxygen free radical injury,stabilizing myocardial cellular membrance and inhibition of apoptosis.