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目的:观察冠心宁注射液对大鼠心肌缺血再灌注损伤的保护作用,探讨冠心宁抗心肌缺血再灌注损伤的保护机理。方法:雄性SD大鼠30只随机分成假手术组(C组)、缺血再灌注组(L/R组)、冠心宁治疗组(G组),建立大鼠在体心肌缺血再灌注模型:C组丝线穿过冠状动脉前降支但不结扎,I/R、G组通过结扎心脏左冠状动脉前降支40 min,再灌注60 min制作缺血再灌注损伤动物模型。缺血前30 min,G组经腹腔注射冠心宁注射液10.0ml·kg~(-1),余两组注射等量0.9%氯化钠注射液。测定再灌注60 min后心肌超氧化物岐化酶(SOD)活性及丙二醛(MDA)含量,同时取每组大鼠心肌检测梗死面积,电镜下观察缺血区心肌超微结构变化。结果:与L/R组相比,G组再灌注后60 min心肌MDA含量降低(P<0.01),SOD活性增高(P< 0.01),梗死面积较小(P<0.01),心肌超微结构受损较轻。结论:冠心宁注射液对心肌缺血再灌注损伤有明显的保护作用,其机制与其增强心肌抗氧化作用有关。
Objective: To observe the protective effect of Guanxinning injection on myocardial ischemia-reperfusion injury in rats and to explore the protective mechanism of Guanxinning against myocardial ischemia-reperfusion injury. METHODS: Thirty male Sprague-Dawley rats were randomly divided into sham operation group (C group), ischemia-reperfusion group (L/R group) and Guanxinning treatment group (G group). Model: C group silk thread through the anterior descending coronary artery without ligation, I / R, G group by ligation of the left descending coronary artery left coronary artery for 40 min, reperfusion for 60 min to produce ischemia-reperfusion injury animal model. 30 min before ischemia, Group G was injected intraperitoneally with Guanxinning Injection (10.0 ml·kg -1 ), and the other two groups were injected with equal volume of 0.9% sodium chloride injection. The activities of superoxide dismutase (SOD) and malondialdehyde (MDA) in the myocardium were measured 60 min after reperfusion. At the same time, the myocardial infarct size was measured in each group and the myocardial ultrastructure was observed under electron microscope. RESULTS: Compared with L/R group, the content of MDA in myocardial tissue was decreased (P<0.01), the activity of SOD was increased (P<0.01), the infarct size was smaller (P<0.01), and myocardial ultrastructure was observed 60 min after reperfusion in G group. Damage is lighter. Conclusion: Guanxinning injection has obvious protective effect on myocardial ischemia-reperfusion injury, and its mechanism is related to its anti-oxidation effect.