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氟伐他汀对兔心肌缺血再灌注损伤的防治效应
引用本文:戴淑华,蒋学俊,李建军,陈莉,秦晋梅.氟伐他汀对兔心肌缺血再灌注损伤的防治效应[J].中国病理生理杂志,2006,22(2):295-298.
作者姓名:戴淑华  蒋学俊  李建军  陈莉  秦晋梅
作者单位:1武汉大学人民医院心内科, 湖北 武汉 430060; 2 清华大学心血管病研究所, 北京 100016
摘    要:目的:观察氟伐他汀对心肌缺血再灌注损伤的防治作用及对心肌ICAM-1 mRNA表达的影响。 方法: 24只日本大耳白兔,随机分3组,假手术组、对照组、处理组(给予氟伐他汀10 mg·kg-1·d-1喂服1周),所有动物在手术前检测血脂,对照组和处理组复制缺血再灌注模型,假手术组只穿线不结扎。监测血流动力学指标,检测血清乳酸脱氢酶(LDH)和肌酸激酶(CK)的活性。RT-PCR检测缺血区及假手术组对应区域心肌ICAM-1 mRNA的表达。 结果: 各组动物在手术前1 d血脂指标无统计学差异;缺血开始后处理组各时点左室舒张末压(LVEDP)小于对照组(P<0.05),左室内压变化最大速率(±dp/dtmax)大于对照组(P<0.05);他汀组LDH-1、CK、CKMB活性均显著小于对照组(均为P<0.01);他汀组心肌组织ICAM-1 mRNA表达显著低于对照组(P<0.01),假手术组表达最少。 结论: 氟伐他汀预处理能减轻心肌缺血再灌注损伤,其机制可能与抑制炎症反应有关。

关 键 词:氟伐他汀  再灌注损伤  胞间粘附分子1  心肌  
文章编号:1000-4718(2006)02-0295-04
收稿时间:2004-06-21
修稿时间:2004-06-212004-11-01

Protective effect of fluvastatin on ischemic reperfused myocardium in rabbits
DAI Shu-hua,JIANG Xue-jun,LI Jian-jun,CHEN Li,OIN Jin-mei.Protective effect of fluvastatin on ischemic reperfused myocardium in rabbits[J].Chinese Journal of Pathophysiology,2006,22(2):295-298.
Authors:DAI Shu-hua  JIANG Xue-jun  LI Jian-jun  CHEN Li  OIN Jin-mei
Institution:1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; 2 Research Centre of Cardiology, Qinghua University, Beijing 100016, China
Abstract:AIM: To investigate the protective effect of fluvastatin and its influence on ICAM-1 mRNA expression in ischemia/reperfusion myocardium of normocholesterolemic rabbits. METHODS: 24 rabbits were divided into three groups randomly and myocardial ischemia/reperfusion model in the rabbit was made. Rabbits were subjected to 45 min of regional myocardial ischemia and 2 h of reperfusion. 10 mg·kg-1·d-1 fluvastatin were administered for one week. Dynamic index of blood flow was recorded and analyzed. Serum activity of CK, CKMB, LDH and LDH-1 were measured. The expression of ICAM-1 mRNA in ischemic myocardium was detected with semi-quantitative RT-PCR. RESULTS: In comparison with control group, pretreatment with fluvastatin decreased LVEDP at the whole observed duration, and spontaneously increased ±dp/dtmax. Serum activities of CK, CKMB and LDH-1 in control group were significantly higher than those in sham group, but heavily reduced in fluvastatin group. Increased expression of ICAM-1 mRNA due to ischemia reperfusion was reduced significantly in fluvastatin group compare to control group. CONCLUSION: Pretreatment of fluvastatin may reduce inflammation reaction in reperfused myocardium, and this may contribute to its protective effect against experimental myocardial ischemia reperfusion injury.
Keywords:Fluvastatin  Reperfusion injury  Intercellular adhesion molecule-1  Myocardium
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