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目的 :探讨黄芪的心肌保护作用机制。方法 :应用兔离体心肌缺血再灌注损伤模型 ,在Thomas液中加入黄芪注射液 ,检测冠脉流量、冠脉回流液中肌钙蛋白 T和腺苷释放、心肌组织中的MDA及外部 5′ 核苷酸酶的活性。结果 :黄芪能有效地保护外部 5′ 核苷酸酶的活性 (P <0 .0 5 ) ;能使腺苷释放明显增加 (P <0 .0 5 ) ;能使冠脉流量明显增加 (P <0 .0 5 ) ,能明显降低冠状循环阻力 (P <0 .0 5 ) ;能使MDA含量明显减少 (P <0 .0 5 ) ;能使肌钙蛋白 T释放明显减少 (P <0 .0 5 )。结论 :在心肌缺血再灌注过程中 ,保护心肌细胞外部 5′ 核苷酸酶的活性 ,使内源性腺苷释放明显增加可能是黄芪减轻心肌缺血再灌注损伤的重要机制之一。
Objective: To explore the mechanism of myocardial protection of Astragalus membranaceus. METHODS: Rabbit isolated myocardial ischemic reperfusion injury model was used. Astragalus membranaceus injection was added to Thomas solution to detect coronary artery flow, troponin T and adenosine release in coronary blood flow, MDA in myocardial tissue and external 5 ’nucleotidase activity. Results: Astragalus can effectively protect the activity of external 5′ nucleotidase (P < 0.05), increase the release of adenosine (P <0.05), and significantly increase coronary flow (P < 0.05). <0.5), can significantly reduce the coronary circulatory resistance (P <0. 0 5); can significantly reduce the MDA content (P <0.05); can significantly reduce the release of troponin T (P <0 .0 5 ). Conclusion: In the process of myocardial ischemic reperfusion, protecting the activity of the 5′-nucleotidase from the myocardium and increasing the release of endogenous adenosine may be one of the important mechanisms of astragalus in reducing ischemia-reperfusion injury.