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为探讨黄芪生脉有效部位(HQSM)治疗心肌缺血的机制,将84只大鼠随机分成7组:正常对照组、模型对照组、HQSM组(210mg/kg、150mg/kg、105mg/kg)、阳性对照组(黄芪生脉饮、地奥心血康)。除正常对照组外,其余各组大鼠尾静脉两次给予垂体后叶素造成急性心肌缺血模型,依法测定各组大鼠心肌ATPase活性、血清中Ca2+含量。结果:HQSM能不同程度地使大鼠心肌Na+-K+-ATPase、Mg2+-ATPase、Ca2+-ATPase活性升高(P<0.05),HQSM150mg/kg能使大鼠心肌Na+-K+-ATPase活性升高(P<0.05);各组大鼠血清Ca2+浓度无明显变化。结论:HQSM抗垂体后叶素所致心肌缺血的作用机制之一可能是增强心肌细胞ATP酶活性从而减少心肌细胞内钙,而不是通过影响血清内钙含量。
In order to investigate the mechanism of HQSM treatment of myocardial ischemia, 84 rats were randomly divided into 7 groups: normal control group, model control group, and HQSM group (210 mg/kg, 150 mg/kg, 105 mg/kg). Positive control group (Huangxi Shengmaiyin, Dioxinxuekang). In addition to the normal control group, the rat model of acute myocardial ischemia induced by pituitrin was given twice in the tail vein of each group. Rats’ myocardial ATPase activity and serum Ca2+ content were determined according to the law. Results: HQSM could increase the activities of Na+-K+-ATPase, Mg2+-ATPase and Ca2+-ATPase in myocardium in different degrees (P<0.05). HQSM150mg/kg could increase the activity of Na+-K+-ATPase in myocardium of rats. P<0.05); There was no significant change in serum Ca2+ concentration in each group. Conclusion: One of the mechanisms of HQSM’s effect on pituitrin-induced myocardial ischemia may be to increase the activity of ATPase in cardiomyocytes and thus reduce intracellular calcium in cardiomyocytes, instead of affecting the serum calcium content.