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目的 :观测芪丹通脉片 (QDTMT)急性心肌缺血损伤的影响 .方法 :用SD大鼠皮下注射异丙肾上腺素 (Iso,5mg·kg-1)诱导心肌缺血模型 ,观测心肌线粒体 (Mit)三磷酸腺苷酶(ATPase)活力、Ca2 + 含量 ;在电镜下 ,观察心肌线粒体超微结构的变化 .结果 :QDTMT组Ca2 + ATPase ,Mg2 + ATPase及Ca2 + Mg2 + ATPase活性显著高于模型组 [(4 0 .9± 8.1)vs(2 3.1± 5 .7) ,(4 0 .4± 4 .4 )vs(2 1.7± 6 .6 ) ,(94 .7± 8.6 )vs (6 3.5± 9.5 )mmol·g-1,P <0 .0 5 ];QDTMT组与模型组相比Ca2 + 显著降低 [(7.6± 1.6 )vs(12 .9± 1.3) ,(37.3± 5 .3)vs(73.2± 8.9)mmol·mg-1,P <0 .0 1].同时 ,与对照组相比 ,心肌超微结构的损害明显减轻 .结论 :QDTMT减轻钙超载和保护心肌细胞超微结构的作用 ,可能是其改善心肌缺血的作用机制之一 .
OBJECTIVE: To observe the effect of Qidan Tongmai Tablet (QDTMT) on acute myocardial ischemia injury. METHODS: Myocardial ischemia model was induced by subcutaneous injection of isoproterenol (Iso, 5 mg·kg-1) in SD rats, and myocardial mitochondria were observed. Mitochondrial adenosine triphosphatase (ATPase) activity and Ca2 + content were observed under electron microscope. Changes of ultrastructure of myocardial mitochondria were observed. Results: The activities of Ca2 + ATPase, Mg2 + ATPase and Ca2 + Mg2 + ATPase in QDTMT group were significantly higher than those in model group [ (4 0 .9± 8.1) vs (2 3.1 ± 5 .7), (4 0 .4 ± 4 .4) vs (2 1.7 ± 6 .6), (94 .7 ± 8.6) vs. (6 3.5 ± 9.5) mmol·g-1, P <0.05; the QDTMT group showed a significant decrease in Ca2+ compared with the model group [(7.6±1.6) vs (12.9± 1.3), (37.3±5.3) vs (73.2 ± 8.9) mmol·mg-1, P <0.01. At the same time, compared with the control group, the damage of myocardial ultrastructure was significantly reduced. Conclusion: QDTMT reduces calcium overload and protects the ultrastructure of myocardial cells. The effect may be one of the mechanisms for improving myocardial ischemia.