氯丙嗪对大鼠缺血性心脏的保护作用及其机制探讨

Protective effect of chlorpnomazine on ischemic heart of rats and its mechanisms

本文研究了氯丙嗪对急性心肌梗塞(MI)大鼠缺血心脏的保护作用及其机制。30只SD雌性大鼠被分为三组:心肌缺血组(结扎冠状动脉造成心肌缺血),缺血+氯丙嗪治疗组及假手术对照组。三组均于术后2小时取材。与假手术对照组相比,缺血组心肌缺血区超微结构发生明显损害;血清CPKmb、血清皮质醇及血清MDA分别较对照组升高了67%、77%和25%(P<0.05);缺血区及非缺血区MDA均明显升高(P<0.05)并伴随SOD降低(P<0.05)。给予氯丙嗪后缺血区心肌超微结构及上述各指标均有一定改善或接近对照组水平。本结果表明:氯丙嗪对缺血心肌具有保护作用,其可能与氯丙嗪的抗应激或/和抗脂质过氧化作用有关。

Protective effects of chlorpromazine on ischemic heart and its mechanisms were investigated in rats with acute myocardial infarction (MI). 30 SD female rats were divided into three groups. the ischemia group, being subjected MI by coronary ligation, the MI+chlorpromazine group and the control. All samples were taken at 2 hours after operation. The ischemia group, as compared to the control, showed remarkable ultrastructural damage in ischemic myocardium and significant increases in serum CPKmb by 77%, serum cortisol by 67% and serum malondialdehyde (MDA) by 25%(P<0.05) In both ischemic and non-ischemic myocardium of the MI group, there were increase in MDA content and decrease in superoxide dismutase (SOD) activity (P<0.05). The ultrastructure in the ischemic area and the indexes mentioned about were significantly alleviated or tend towards those of the control by chlorpromazine supplements. The results demonstrate that chlorpromazine has a protective effect on ischemic and nonischemic myocardium, which is probably resulted from its anti-stress or/and anti-peroxidation.