大鼠离体心脏急性冬眠心肌模型的建立

Acute hibernating myocardium in isolated rat heart

利用悬浮人类红血球的改良K-H液灌流大鼠离体等容收缩心脏,建立了急性冬眠心肌模型,缺血期间冠状动脉流量下降80%.结果表明,缺血30分钟时,左室内收缩峰压、dp/dt max、—dp/dt max分别降到对照组的44%、33%和26%(P均<0.05),缺血期间保持恒定,再灌注30分钟完全恢复.缺血90分钟,心肌ATP、磷酸肌酸(Crp)及糖原含量明显降低(P均<O.05),再灌注30分钟,CrP及糖原含量恢复.心肌乳酸代谢也由正常时摄取乳酸转变为释放乳酸(P<0.05),再灌注30分钟后恢复.缺血90分钟时,心尖部透射电镜检查未发现不可逆损害.以上结果表明,建立的模型符合急性冬眠心肌的特点.

We set up an animal model of acute hibernating myocardium isolated rat heart. which were perfused with human red blood cell-enhanced modified K-H buffer,were used. During ischemia,coronary flow were reduced to 20%. The results show: At 30 minutes of ischemia,left ventircular peak systolic pressure,+dp/dt max and - dp/dt max were decreased to 44% ,33% and 26% (P<0. 05) of that of control group,those measure were stable during ischemia and were completely restored by reperfusion. At 90 minutes ischemia, myocardial ATP,creatine phosphate (CrP) and glycogen contents were all depressed (P<0. 05) ,and there was net lactate production. At 30 minutes of reperfusion,however,myocardial ATP and glycogen were restored,and lactate consumption was nestored,too. At 90 minutes of ischemia,no irreversible ultrastructual changes was found in apical part of the heart. The results suggest that the present model is in keeping with the definitian of acute hibernating myocardium.