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目的观察阿托伐他汀(ATV)预处理的心肌保护效应,探讨诱导型一氧化氮合酶(iNOS)和线粒体膜 ATP 敏感性钾通道(K_(ATP))在其中的作用以及这两个环节的相互关系。方法将兔随机分成缺血再灌注模型对照组(对照组)、ATV 组、ATV 复合 iNOS 阻断剂 S-甲基异琉脲硫酸盐组(ATV+SMT 组)、S-甲基异琉脲硫酸盐组(SMT 组)、ATV 复合线粒体膜 K_(ATP)通道阻断剂5-羟癸酸组(ATV+5-HD 组)、5-羟癸酸组(5-HD)组。进行40 min 局部缺血和240 min 再灌注,观察各组心肌梗死范围、血液生物化学、一氧化氮合酶、线粒体 ATP 合成能力。结果 3天阿托伐他汀预处理(10 mg·kg~(-1)·d~(-1))使心肌梗死范围、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶同工酶(LDH-1)分别下降26.3%、31.4%、19.1%,使 iNOS、线粒体 ATP 合成能力分别提高102.6%和46.8%。ATV+SMT 组心肌梗死范围、CK-MB、LDH-1、iNOS、线粒体 ATP 合成能力和对照组无明显差异。ATV+5-HD 组心肌梗死范围、CK-MB、LDH-1、线粒体 ATP 合成能力和对照组无明显差异,ATV+5-HD 组 iNOS 和 ATV 组相似,均明显高于对照组(P<0.01)。结论阿托伐他汀预处理通过上调 iNOS 和激活线粒体膜 K_(ATP)产生心肌保护作用,且 iNOS 是线粒体膜 K_(ATP)的上游途径。
Objective To observe the protective effect of atorvastatin (ATV) preconditioning on myocardium and to explore the role of inducible nitric oxide synthase (iNOS) and mitochondrial ATP-sensitive potassium channel (K_ (ATP) The relationship between. Methods Rabbits were randomly divided into 4 groups: control group, ATV group, ATV combined iNOS blocker S-methyl isothiocyanuric acid sulfate group (ATV + SMT group), S-methyl isothiourea (SMT group), ATV complex mitochondrial membrane K (ATP) channel blocker 5-hydroxydecanoic acid group (ATV + 5-HD group) and 5-hydroxydecanoic acid group (5-HD group). 40 min ischemia and 240 min reperfusion were performed. The extent of myocardial infarction, blood biochemistry, nitric oxide synthase and mitochondrial ATP synthesis were observed. Results 3 days of atorvastatin pretreatment (10 mg · kg -1 · d -1) decreased myocardial infarct size, CK-MB and lactate dehydrogenase (LDH-1) decreased by 26.3%, 31.4% and 19.1%, respectively, which increased the iNOS and mitochondrial ATP synthesis by 102.6% and 46.8% respectively. Myocardial infarction area, CK-MB, LDH-1, iNOS and mitochondrial ATP synthesis capacity in ATV + SMT group were not significantly different from those in control group. The ATV + 5-HD group showed no significant difference in the myocardial infarct size, CK-MB, LDH-1 and mitochondrial ATP synthesis compared with the control group. The iNOS and ATV groups in ATV + 5-HD group were significantly higher than those in the control group (P < 0.01). Conclusions Atorvastatin preconditioning can induce myocardial protection by up-regulating iNOS and activating mitochondrial membrane K_ (ATP), and iNOS is the upstream pathway of mitochondrial membrane K_ (ATP).