Libersa C, Honoré E, Adamantidis M, Rouet E, Dupuis B, Challice C
Presse Med. 1986 Oct 16;15(35):1765-9.
Cardioprotection is a new concept proposed for clinical situations as myocardial infarction and cardiac surgery. Cardioprotective effects are mainly evaluated in patients by enzymatic, electrocardiographic and sometimes histological findings. The aim of this work was to study the effects of trimetazidine on guinea-pig ventricular myocardium submitted in vitro to conditions mimicking ischaemia. A three step procedure was used: a period of stabilization of 180 minutes under control conditions, then a period of 60 minutes under ischaemic conditions, and last a replacement into control conditions perfusion (30 minutes). Trimetazidine was added in the superfusion during the last hour of stabilization and maintained during the ischaemic and the reperfusion periods. Electrical activities (micro-electrodes) and creatine phosphokinase activity in the effluent were monitorized. Trimetazidine (10(-6) M) prolonged during the ischaemic phase the duration of decremental response and improved electrical recovery during reperfusion. Moreover, trimetazidine (10(-6) M) reduced creatine phosphokinase leakage during ischaemia. The effects of trimetazidine were compared to those observed with calcium channel antagonists in the same model. Thus slowing of enzyme leakage and electrical improvement observed under trimetazidine are compatible with a so-called cardioprotective effect.
心脏保护是针对心肌梗死和心脏手术等临床情况提出的新概念。心脏保护作用主要通过酶学、心电图检查，有时也通过组织学检查结果在患者中进行评估。本研究的目的是研究曲美他嗪对体外模拟缺血条件下豚鼠心室心肌的影响。采用了三步程序：在对照条件下稳定180分钟，然后在缺血条件下60分钟，最后恢复到对照条件下灌注（30分钟）。在稳定期的最后一小时向灌流液中加入曲美他嗪，并在缺血期和再灌注期持续添加。监测流出液中的电活动（微电极）和肌酸磷酸激酶活性。曲美他嗪（10^(-6) M）在缺血期延长了递减反应的持续时间，并改善了再灌注期间的电恢复。此外，曲美他嗪（10^(-6) M）减少了缺血期间肌酸磷酸激酶的泄漏。将曲美他嗪的作用与在同一模型中观察到的钙通道拮抗剂的作用进行了比较。因此，在曲美他嗪作用下观察到的酶泄漏减慢和电活动改善与所谓的心脏保护作用相符。
