【摘要】 目的:观察阿托伐他汀(ATV)对心肌缺血再灌注损伤的影响以及诱导型一氧化氮合酶(iNOS)在其中的作用。方法:将健康雄性新西兰大耳白兔随机分成模型对照组、ATV组、ATV+S-甲基异琉脲硫酸盐(SMT)组、SMT组,每组8只。进行40min局部缺血和240min再灌注,观察各组血流动力学、血液生物化学及一氧化氮合酶的变化。结果:缺血再灌注使左室发展压(LVDP)和压力上升最大速率(+dp/dtmax)分别下降24.6%和35.3%;3dATV预处理(10mg.kg-1.d-1)使缺血再灌注后LVDP和+dp/dtmax的下降幅度分别减小21.7%和41.3%,使心肌型肌酸激酶同功酶(CK-MB)和乳酸脱氢酶(LDH-1)分别降低31.4%和19.1%,使iNOS上升102.6%;ATV+SMT组LVDP和+dp/dtmax的下降幅度、CK-MB、LDH-1、iNOS均和模型对照组无明显差异。结论:ATV预处理通过上调iNOS减轻心肌缺血再灌注损伤。更多还原

【Abstract】 AIM:To observe the effect of atorvastatin(ATV) on myocardial ischemia-reperfusion injury and the role of inducible nitric oxide synthase (iNOS). METHODS: The rabbits were randomly divided into control group, ATV group, ATV+S-Methylisothiourea sulfate (SMT) group, SMT group. All rabbits were subjected to 40 min ischemia and 240 min reperfusion. The hemodynamic variables, CK-MB, LDH-1 and nitric oxide synthase were detected after reperfusion. RESULTS: LVDP and +dp/dtmax decreased by 24.6% and 35.3% respectively following ischemia-reperfusion. Pre-treated by ATV (10 mg·kg-1·d-1) for three days, LVDP and +dp/dtmax decreased by 21.7% and 41.3%, CK-MB and LDH-1 by 31.4% and 19.1% and iNOS increased to 102.6%. The reduction of LVDP and +dp/dtmax, CK-MB, LDH-1 and iNOS in ATV+SMT group was no statistically significant with those in control group. CONCLUSION: ATV pretreatment protected myocardial ischemia-reperfusion injury by upregulating iNOS.更多还原