Abatement effect of myocardial injury by ischemic postconditioning during acute ischemia/reperfusion in rabbits

AIM: To study the early protective effect of myocardium by ischemic postconditioning on ischemic myocardium in rabbits. METHODS: Fifty six rabbits were included in this study and were randomly divided into control group (Con, n=28) and ischemic postconditioning group (Post-con, n=28). An in vivo rabbit model of acute myocardial infarction/reperfusion was established with left ventricle branch (LVB) occluded for 40 min and reperfused for 3 h. In Con, there was no intervention. In Post-con, at the start of R, three cycles of 30 sec R and 30 sec LVB re-occlusion preceded the 3 h of R. ECG was observed during the first 2 h of reperfusion. Plasma malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) were measured at baseline, end of ischemia, and at 1h and 3 h of reperfusion. At the end of the experiment, the rabbits of Con and Post-con were randomly divided into two equal subgroups. The rabbits in one subgroup were killed to determine myocardial infarct size determined by dual staining with triphenyltetrazolium chloride and Evans blue dye. Cardiac structural and functional changes were evaluated with transthoracic echocardiography (TTE) in the other subgroup 4 weeks after myocardial infarction. RESULTS: Myocardial reperfusion was much more effective in Post-con group vs. Con (P<0.05) and myocardial infarct size was significantly reduced in Post-con vs. Con (P<0.05). Plasma MDA at 1 h of reperfusion was significantly less and plasma SOD and GSH-PX were higher in Post-con vs. Con (P<0.05). After 4 weeks, TTE showed that the extent of posterior left ventricular (PLV) wall and its thickenness in systolic period as well as left ventricular fractional shortening (LVFS) and left ventricular ejection fraction (LVEF) were significantly improved in Post-con vs. Con (P<0.05). CONCLUSION: Ischemic postconditioning reduces acute myocardial ischemia/reperfusion injury by inhibiting oxyradical activation at the beginning of reperfusion, which improves the effective perfusion on ischemic myocardium and reduces myocardial infarct size and improves left ventricular contractive function.