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目的:探讨洛伐他汀预适应对大鼠心脏急性缺血再灌注中的心肌保护作用及其机制。方法:将 24只SD大鼠随机分为3组(每组均8只):模型对照组(C组); 洛伐他汀组( L组),胃管直接灌注洛伐他汀 15 mg·kg-1·d-12周;洛伐他汀复合L 硝基精氨酸甲酯(L NAME)组(N组),洛伐他汀直接灌胃 2 周同时腹腔注射L NAME 30 mg·kg-1·d-1;2周后建立体内急性缺血再灌注心脏模型,监测缺血再灌注前后血流动力学各项指标,同时观察各组血脂水平及其血浆中丙二醛(MDA) 、心肌组织内超氧化物歧化酶(SOD)变化情况。结果: L组和N组较C组心率明显变慢(P<0.01),缺血再灌注心律失常消失和再灌注时-dp/dtmax下降明显改善(P<0.05);同时各项血脂指标不变,洛伐他汀能明显减少再灌注时血浆中MDA生成, 并且提高心肌组织SOD活性(P<0.05)。结论:洛伐他汀预适应对体内大鼠心脏急性缺血再灌注时具有非降脂外的心肌保护作用,其机制除与其增加一氧化氮(NO)合成相关外,可能还有其他物质或途径参与。
Objective: To investigate the protective effect of lovastatin preconditioning on cardiac myocytes during acute myocardial ischemia / reperfusion in rats and its mechanism. Methods: Twenty-four Sprague-Dawley rats were randomly divided into 3 groups (8 in each group): model group (group C), lovastatin group (group L), lovastatin 15 mg · kg- 1 · d-12 weeks; lovastatin L-NAME group (group N), lovastatin 2 weeks after intragastric administration of L-NAME 30 mg · kg-1 · d -1; 2 weeks after establishment of acute ischemia-reperfusion heart model in vivo, before and after ischemia-reperfusion hemodynamic monitoring of various indicators, at the same time to observe the levels of blood lipid and plasma malondialdehyde (MDA), myocardial tissue Changes of superoxide dismutase (SOD). Results: The heart rate of group L and group N were significantly lower than that of group C (P <0.01), the disappearance of arrhythmia of ischemia-reperfusion and the decrease of -dp / dtmax at reperfusion were significantly improved (P <0.05); meanwhile, Lovastatin can significantly reduce the plasma MDA level during reperfusion, and increase the activity of SOD in myocardium (P <0.05). CONCLUSION: Lovastatin preconditioning has protective effects on myocardium during acute ischemia-reperfusion injury in vivo and its mechanisms may be related to the addition of nitric oxide (NO) synthesis and other substances or pathways participate.