THE SIGNAL MECHANISM OF THE PROTECTION OF ISCHEMIC POSTCONDITIONING ON MYOCARDIUM DURING ISCHEMIA/REPERFUSION IN RABBIT HEART

Objective:To investigate the signal mechanism of the protection of ischemic postconditioning on myocardium during ischemia/reperfusion in rabbit.Methods: All animals were randomly divided into three groups:(1)sham group;(2)I/R group,(3)I-PostC group.In group3,when the LAD was occlused for 24min,the femoral arteries were occlused for 5min,and then were unclamped for 1min,and reperfused to 180min All groups underwent 30min of coronary occlusion followed by 180min of reperfusion except Group1.At the end of the reperfusion,infarct size(IS)and area at risk(AAR) were defined by Evans and TTC staining.Cardiac myocyte apoptosis was defined by Terminal deoxynucleotidyl Transferase mediated dUPT nick-end labeling(TUNEL)method.The levels of BCL-2 and P-stat3 activity were determined by Westen Blot analysis.Results:Myocardial ischemic postconditioning and significantly(P0.05)reduced infarctsize(19.9±5.4%) compared with I/R group(29.9±4.6%).In Group 2,ischemia/reperfusion caused significant cardiac myocyte apoptotic death.Ischemic postconditioning and morphine produced a significantly anti-apoptotic effect as evidenced by a marked reduction of apoptotic index in I/Rgroup.The activity of BCL-2 and P-stat3 in Group3 was higher than that of on Group2(P0.05).Conclusions: Ischemic postconditioning can inhibit cardic myocyte apoptotic death,and promote the activity of BCL-2 and P-stat3 in myocardium during ischemia reperfusion,which is likely activitied by JAK-STAT signal pathway,and may be one of the molecular mechanisms of ischemic postconditioning on cardioProtection.