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目的:观察洋参二醇皂苷注射液(IPQDS)对大鼠急性心肌梗死的保护作用及其机制。方法:采用大鼠结扎左冠状动脉前降支制备急性心肌梗死模型,计算急性心肌梗死24 h后的心肌梗死面积(M IS),测定血清肌酸磷酸激酶(CK)、乳酸脱氢酶(LDH)、天门冬氨酸氨基转换酶(AST)、超氧物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力及丙二醛(MAD)、一氧化氮(NO)含量,观察全血低切、中切、高切黏度及血浆黏度,并测定血小板黏附与聚集功能。结果:IPQDS可明显缩小急性心肌梗死大鼠的M IS,降低血清CK,LDH,AST活性及MAD含量,提高血清SOD、GSH-Px活性及NO含量,亦可使全血低、中、高切黏度,血浆黏度及血小板聚集功能明显降低,对血小板黏附功能无明显影响。结论:IPQDS对大鼠急性心肌梗死具有明显保护作用,其机制可能与提高体内抗氧化酶活性,减少自由基对心肌的氧化损伤,纠正心肌缺血时的血液高黏滞状态,防止血栓形成等作用有关。
Objective: To observe the protective effect of IPQDS on acute myocardial infarction in rats and its mechanism. METHODS: The acute myocardial infarction model was established by ligating the left anterior descending coronary artery in rats. The myocardial infarct size (M IS) was calculated after 24 h of acute myocardial infarction. Serum creatine kinase (CK) and lactate dehydrogenase (LDH) were measured. ), aspartate aminotransferase (AST), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activity and malondialdehyde (MAD), nitric oxide (NO) Content, observe low-cut, mid-cut, high-cut viscosity and plasma viscosity of whole blood, and measure platelet adhesion and aggregation. Results: IPQDS can significantly reduce the M IS in acute myocardial infarction rats, reduce serum CK, LDH, AST activity and MAD content, increase serum SOD, GSH-Px activity and NO content, also can make whole blood low, medium and high cut Viscosity, plasma viscosity and platelet aggregation were significantly reduced, and there was no significant effect on platelet adhesion. Conclusion: IPQDS has obvious protective effect on acute myocardial infarction in rats. Its mechanism may be to increase antioxidase activity in vivo, reduce free radical oxidative damage to myocardium, correct hyperviscosity in myocardial ischemia, prevent thrombosis, etc. Role related.