促红细胞生成素对大鼠心肌缺血再灌注损伤的影响

目的:观察促红细胞生成素(erythropoietin,EPO)对大鼠心肌缺血再灌损伤的影响,并探讨机制.方法:以左冠状动脉前降支(LAD)穿线结扎法制备心肌缺血模型,松开结扎线造成再灌注.45只SD大鼠随机分成5组:①假手术组,②缺血再灌注组,③磷脂酰肌醇-3-激酶(PI3K)的高选择性阻断剂LY294002组,④EPO 组和⑤EPO+LY294002组.观察心电图Ⅱ导联心律失常发生情况,进行室性心律失常评分;电镜观察心肌细胞超微结构;以TUNEL法检测细胞凋亡;检测血清肌酸磷酸激酶同工酶(CK-MB)和肌钙蛋白I(cTnI)水平.结果:EPO能降低心律失常评分(P<0.01),减轻心肌细胞超微结构损伤,减少细胞凋亡(P<0.01),降低血清CK-MB和cTnI水平(P<0.01),但这些作用可被预先给予的LY294002所减弱.结论:EPO能减轻心肌缺血再灌注损伤, PI3K参与其信号转导.

Effect of erythropoietin on myocardial ischemia-reperfusion injury in rats

Objective:To observe the effect of erythropoietin(EPO) on myocardial-reperfusion injury in rats, discuss the mechanism involved.Method:The left anterior descending branch of coronary artery (LAD) of rats was ligated for 30 min and then loosed for 3 h to establish ischemia/reperfusion heart model. 45 SD rats were randomly divided into 5 groups:Sham operation group (group SHAM),and 4 experimental groups:group IR,group LY,group EPO and group EPO+LY. The arrhythmias were monitored during experiment, to score the ventricular arrhythmias. The change of cardiac ultrastructure were examed by transmission electron microscope. Myocardia1 cells apoptosis were estimated by in situ nick end 1abeling (TUNEL)method. The levels of serum CK-MB and cTnI were detected. Result: EPO treatment decreased the arrhythmia score(P<0.05), protected the ultrastructure of myocardium, decreased apoptotic index(P<0.01), decreased the levels of serum CK-MB and cTnI(P<0.01). LY294002 attenuated the effect of EPO. Conclusion:EPO treatment prevented against myocardial ischemia-reperfusion injury in rats,the cardioprotection by EPO required the PI3K pathway.