Pfeffer J M, Pfeffer M A, Braunwald E
Circulation. 1987 Jan;75(1 Pt 2):I149-55.
To determine whether the hemodynamic profile of chronic heart failure secondary to myocardial infarction could be altered, captopril was administered to female Wistar rats 3 weeks after coronary artery ligation and continued for 3 months. Captopril reduced left ventricular mass, prevented the increase in right ventricular mass observed with increasing infarct size, lessened the increase in left ventricular end-diastolic pressure, and reduced mean arterial pressure and total peripheral resistance, whereas cardiac output and heart rate were maintained. The end-diastolic volume of treated rats with moderate infarcts was significantly less than that of untreated rats, and therefore the ejection fraction index was significantly increased. In rats given captopril until death or for a period of up to 1 year, survival was significantly prolonged, particularly in those rats with moderate-sized infarcts.
为了确定心肌梗死后慢性心力衰竭的血流动力学特征是否可以改变，在冠状动脉结扎3周后给雌性Wistar大鼠服用卡托普利，并持续3个月。卡托普利可减轻左心室重量，防止随着梗死面积增大而出现的右心室重量增加，减轻左心室舒张末期压力的升高，并降低平均动脉压和总外周阻力，而心输出量和心率保持不变。中度梗死的治疗组大鼠的舒张末期容积明显小于未治疗组大鼠，因此射血分数指数显著升高。在给予卡托普利直至死亡或长达1年的大鼠中，生存期显著延长，尤其是那些中度梗死的大鼠。
