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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。
This study investigated the protective effect of chlorpromazine on ischemic heart in rats with acute myocardial infarction (MI) and its mechanism. Thirty SD female rats were divided into three groups: myocardial ischemia group (myocardial ischemia caused by ligation of coronary artery), ischemic + chlorpromazine treatment group and sham operation control group. Three groups were drawn 2 hours after surgery. Compared with the sham operation group, the ultrastructure of ischemic myocardium in the ischemic group was significantly impaired. The levels of serum CPKmb, serum cortisol and serum MDA increased by 67%, 77% and 25% respectively (P <0.05 ). MDA in ischemic area and non-ischemic area increased significantly (P <0.05) and accompanied with decreased SOD (P <0.05). After administration of chlorpromazine, ischemic myocardial ultrastructure and the above indicators have improved or close to the control group. The results show that: chlorpromazine has a protective effect on ischemic myocardium, which may be related to chlorpromazine anti-stress and / or anti-lipid peroxidation.