rhBNP对急性心肌梗死再灌注后急性期细胞因子、心肌凋亡的实验研究

目的：通过构建急性心肌梗死（AMI）再灌注犬模型后,冠脉及静脉应用rhBNP,观察急性缺血-再灌注损伤中细胞因子的变化及对心肌细胞凋亡的影响。方法：选用成年杂种犬15只,置入PTCA球囊至左前降支（LAD）或左旋支（LCX）,封堵90min;后球囊撤出完成AMI再灌注模型。成功制备12只AMI再灌注模型,随机分为rhBNP组和对照组。冠脉及静脉应用rhBNP或生理盐水60min。分别于术前及术后采血,检测血浆BNP、ET-1水平;病理检测凋亡心肌细胞含量。结果：对照组及rhBNP组实验犬AMI后90min冠脉血BNP水平较术前显著升高（均P〈0.01）;对照组AMI后210min静脉血BNP水平较术前显著升高（P〈0.01）。对照组及rhBNP组实验犬AMI后90min冠脉血ET-1水平较术前有所升高（P〉0.05或P〈0.05）;对照组AMI后210min静脉血ET-1水平较术前显著升高（P〈0.01）。rhBNP组凋亡指数显著减小[（17.5±2.9）%与（24.5±3.6）%,P〈0.01]。结论：AMI再灌注后即刻冠脉及静脉应用rhBNP可影响缺血-再灌注细胞因子变化,减少心肌细胞凋亡,对心脏有保护作用。

Experimental study of infusion of rhBNP about cytokines and myocardial apoptosis in acute myocardial infarction reperfusion

Objective：To observe the changes of cytokines of ischemic perfusion damage and apoptosis after infusion of rhBNP in PTCA dog models of acute myocardial infarction （AMI）. Methods：15 adult dogs were selected,PTCA sacculus proprius was inserted into LAD or LCX for 90 min,then the sacculus proprius was taken out to complete the AMI reperfu-sion model. 12 PTCA dog models of AMI were successfully established and randomly divided into rhBNP group and control group. Coronary artery and vein were treated with rhBNP or NS for 60 min. Plasma BNP and ET-1 were respectively det ected at pre-operation and post-operation. The apoptosis index of myocardium was detected after AMI. Results：Coronary plasma BNP was significantly increased after occlusion 90 min later of the two groups compared with the pre-operation （P〈0.01）. Plasma BNP after occlusion 210 min of control group was significantly increased （P〈0.01）. Coronary plasma ET-1 was increased after occlusion 90 min later of the two groups compared with the pre-operation （P〉0.05 or P〈0.01）. The plasma ET-1 after occlusion 210 min of control group was obviously increased （P〈0.01）. AI of the two groups was significiantly decreased [（17.5±2.9）% vs （24.5±3.6）%,P〈0.01]. Conclusion：The coronary and intravenous infusion of rhBNP after AMI and reperfusion may reduce the damage of ischamic reperfusion,decrease the myocardial cell apoptosis and play a role in protecting heart.