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采用大鼠异丙肾上腺素性心肌梗塞(ISP-MI)模型,进行了氯丙嗪对心肌缺血性膜损伤的保护作用及其机制的研究。结果表明:心肌缺血维心肌匀浆总磷脂明显减少,心肌 FFA 及 MDA显著升高,心肌线粒体膜脂流动性明显降低;与心肌缺血组相比,氯丙嗪处理组心肌匀浆总磷脂显著升高(P<0.05),线粒体膜脂流动性明显增高(P<0.01).心肌 FFA 硬 MDA 显著降低(P<0.01,P<0.05)。提示:氯丙嗪对心肌缺血性膜损伤有保护作用,其机制与抑制 PLA_2活性及抗自由基的作用有关。
The isoprenaline-induced myocardial infarction (ISP-MI) model was used to study the protective effect of chlorpromazine on myocardial ischemic membrane injury and its mechanism. The results showed that the total phospholipids in myocardial homogenate were significantly decreased, myocardial FFA and MDA were significantly increased, and myocardial mitochondrial membrane lipid fluidity was significantly reduced. Compared with myocardial ischemic group, chlorpromazine-treated group myocardial homogenate total phospholipids Significant increase (P <0.05), mitochondrial membrane lipid fluidity was significantly increased (P <0.01). Myocardium FFA hard MDA was significantly reduced (P <0.01, P <0.05). Tip: Chlorpromazine has a protective effect against myocardial ischemic membrane damage, and its mechanism is related to the inhibition of PLA_2 activity and the effect of anti-free radicals.