Effect of Cardiac Ischemic Preconditioning on Myocardium With its Mechanism in Aged Rats

Objective: To explore the impact of Ischemic preconditioning(IPC) in aged experimental rats after myocardial ischemia-reperfusion(I/R) with its mechanism. Methods: A total of 32 Wistar rats at the age of(21-23) months were divided into 4 groups, n=8 in each group. 1 Control group, the rats received cardiac perfusion for 180 min. 2 I/R group, the rats received cardiac perfusion for 30 min, followed by ischemia for 30 min, then reperfusion for 120 min. 3 IPC group, the rats received cardiac perfusion for 10 min, followed by ischemia and reperfusion 2 times(5 min in each time), then ischemia 30 min and reperfusion 120 min. 4 Enhanced IPC group, rats received cardiac perfusion for 10 min, followed by ischemia and reperfusion 4 times(5 min in each time), then ischemia 30 min and reperfusion 120 min. The recovery rate of cardiac output(CO), left ventricular developed pressure(LVDP) and the recovery rate of maximum rise and fall of left ventricular pressure(±dp/dtmax) at(30, 60, 90, 120) min after reperfusion were recorded respectively. The creatine kinase(CK-MB), superoxide dismutase(SOD) activity and malondialdehyde(MDA) content were examined before ischemia and 120 min after reperfusion. The apical peroxisome proliferator-activated receptor γ co-stimulatory factor 1α(PGC-1α) was examined by immuno-histochemistry.Results: The MDA content, CK-MB, SOD activities LVDP and(±dp/dtmax) recovery were similar between IPC group and I/R group, P0.05. While compared with I/R group, the Enhanced IPC group showed decreased CK-MB activity and MDA content, increased SOD activity and CO, LVDP and(±dp/dtmax) recovery rate, all P0.01. The PGC-1α expression was similar between IPC group and I/R group, P0.05. While compared with I/R group, the Enhanced IPC group had increased PGC-1α expression, P0.01.Conclusion: The cardiac IPC was weakened in aged rats which might be because of decreased PGC-1α expression, the enhanced IPC may up-regulate PGC-1α expression and therefore, protect the cardiac tissue in aged experimental rats.