【摘要】 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。更多还原

【Abstract】 Objective To observe the preconditioning cardioprotection of atovastatin（ATV）in rabbits underwent 40 min ischemia and 240 min reperfusion and to explore related mechanisms.Methods The rabbits were randomized divided into Control group,ATV group(10 mg·kg^-1·d^-1for 3 days before ischemia),ATV plus iNOS inhibitor S-methylisothiourea sulfate group（ATV + SMT group）,SMT group, ATV plus mito K_ATP channel blocker 5-hydroxydecanoate group（ATV + 5-HD group）and 5-HD group（n= 16 each group）.The infarction size,CK-MB,LDH-1,nitric oxide synthase and mitochondrial ATP synthesization capacity（[ATP]m）were determined at the end of reperfusion.Results Infarction size, CK-MB,LDH-1 were decreased by 26.3%,31.4%,19.1% and iNOS,[ATP]m increased by 102.6%, 46.8% post ATV compared to control group（all P<0.05）and these effects could be blocked by cotreatment with SMT and 5-HD except the iNOS was not affected by 5-HD.Conclusion The atovastatin preconditioning exerted cardioproteetion by upregulating iNOS and activating mito K_ATP.更多还原