[Effects of trimetazidine on a model of in vitro myocardial ischemia].

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.