| Background Although the prognosis of acute myocardial infarction(AMI) has significantly improved because of the progress of reperfusion therapy(ie,thrombolytic therapy and percutaneous coronary intervention)in the last two decades, it may also have deleterious effects (reperfusion injury),which may offset the benefit of earlier reperfusion even aggravate the damage.The research about the myocardial protection of ischemia /reperfusion(I/R) injury have been developing from ischemic preconditioning(IPC), pharmacologic preconditioning(PPC),remote ischemic preconditioning (RPC), to current hot point :ischemic postconditioning(IP)in recent years.Now IP have been proved to reduce infarct size,reperfusion malignant arrhythmia and been approach for the mechanisms in some research about rabbit,dog and rat.But domestic rearches about IP start late,and they were not full-scale enough .The reports about the structure and function change of AMI recovery phase were rare . So we plan to carry out the research about IP during the earlier period of reperfusion in rabbits and to demonstrate completely the early protective effect of IP on rabbit's acute myocardial ischemia/reperfusion injury and the mechanisms in the aspect of ECG,arrhythmia,infarct size,plasma MB isoenzyme of creatine kinase (CK-MB),cardiac troponin-I (Tn-I),free radicle,structure and function change.This study will set up a base for IP to be further applied clinically。Objective To study the early protective effect of ischemia postconditioning on rabbit's acute myocardial ischemia/reperfusion (I/R) injury and the mechanism. Methods An in vivo rabbit model of ischemia/reperfusion(I/R) was established by left ventricle branch occludsion for 40 min followed by reperfusion for 180 min.All rabbits enrolled in this study were randomly divided into 2 groups (n=20 in each group): (1)Control:left ventricle branch occlusion and reperfusion only,with no other intervention protocol;(2)Myocardial ischemic postconditioning(IP):after 40min of left ventricle branch occlusion, reperfusion was initiated for 30 s followed by 30s reocclusion.Three cycles of myocardial ischemia (30s) and repefusion(30s) followed the index ischemia/reperfusion protoco1. ECG and arrhythmia scores were observed during the first 2 hr's reperfusion and plasma MB isoenzyme of creatine kinase (CK-MB) activity,cardiac troponin-I (Tn-I) activity,malondialdehyde(MDA)activity,superoxide dismutase (SOD)activity and glutathione peroxidase(GSH-PX) activity were measured at baseline,the end of ischemia,and at 3 h of reperfusion respectively. At the end of the experiment,the rabbits of the control group and the IP group were randomly divided into half respectively. Ten rabbits of each group were made death to determine myocardial infarct size by dual staining with triphenyltetrazolium chloride and Evan'S blue dye.The other rabbits of each group were test cardiac structure and function change(Wall motion, LVEF, LVFS) by transthoracic echocardiography (TTE) four weeks after myocardial infarction.Result Compare with the control group , the average values of S-T segment elevation in leadⅡ,Ⅲ,AVF displayed on the ECG of IP group'rabbit were smaller and the effective power of myocardial reperfusion was much better(P<0.05) .The rate of arrhythmia occurrence and the persistence time of arrhythmia during reperfusion,plasma CK-MB,TnI activity at 3 h 0f reperfusion and myocardial infarct size were significantly reduced in the IP group than that in the control group(P <0.05). Compare with the control group ,the concentration of MDA in plasma at 1 h 0f reperfusion were significantly lower(P <0.05),and the concentration of SOD and GSH-PX in plasma of IP group were higher than that of the control group (P <0.05). AS far as plasma MDA,SOD and GSH-PX at 3 h 0f reperfusion were concerned, there was no significant difference between the control group and IP group (P>0.O5).Four weeks later TTE shows that the extent of posterior left ventricular (PLV) wall and its thickenness in systolic period, LVFS, LVEF were significantly reduced than that in the control group (P <0.05).Conclusion Ischemic postconditioning has protective effect on acute myocardial ischemia /reperfusion injury by inhibiting oxyradical activation at the beginning of reperfusion ,which can improved the effective perfusion on ischemic myocardium, reduce myocardial infarct size and left ventricular contractive function lesion.
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