盐酸法舒地尔后适应对大鼠心肌缺血/再灌注损伤的影响及其机制  

The Potential Mechanisms of Fasudil Hydrochloride on Postconditioning of Acute Myocardial Ischemia/Reperfusion Injury in Rats

作　　者：蒋智慧[1,2] 冯广智[1,2] 钱志勇[1,2] 徐曙东[1,2] 

机构地区：[1]江苏省泰兴市人民医院 [2]蚌埠医学院附属泰兴医院心内科,江苏省泰兴市225400

出　　处：《中国动脉硬化杂志》2013年第3期209-214,共6页Chinese Journal of Arteriosclerosis

基　　金：蚌埠医学院自然科学研究资助项目(Byky1298NF)

摘　　要：目的通过主动脉根部模拟冠状动脉内给药,观察盐酸法舒地尔后适应对大鼠急性心肌缺血/再灌注损伤的保护作用,并探讨其机制。方法 60只SD大鼠随机分为假手术组、缺血再灌注组、PI3K抑制剂组、盐酸法舒地尔组、盐酸法舒地尔+PI3K抑制剂组,每组12只。各组于再灌注180 min后处死大鼠,分别测定心功能参数、血浆心肌酶、细胞凋亡指数和心肌梗死范围。结果盐酸法舒地尔组心肌细胞凋亡指数、心肌梗死范围与缺血再灌注组比较明显减少(P<0.01);给予PI3K抑制剂,盐酸法舒地尔的后适应效应消失,即盐酸法舒地尔+PI3K抑制剂组心肌细胞凋亡指数、心肌梗死范围与盐酸法舒地尔组比较明显增加(P<0.01)。结论盐酸法舒地尔后适应的机制可能与激活PI3K-Akt传导通路有关。Aim To investigate the protective effects of fasudil hydrochloride on postconditioning of acute myocardial ischemia/reperfusion injury, and the potential mechanisms in rats. Methods Sixty rats were randomly divided into 5 groups： sham operation group, ischemia/reperfusion group, an inhibitor of PI3K group, fasudil hydrochloride group, fasudil hydrochloride and an inhibitor of PI3K group. There were 12 rats in each group. Animals were sacrificed after 180 minutes reperfusion to determine heart function parameters, plasma myocardial enzymes, cell apoptosis index and myocardial infarct size. Results The levels of apoptosis index and myocardial infarct size in the fasudil hydrochloride group were significantly lower than in the ischemia/reperfusion group （all P〈0.01）. But using an inhibitor of PI3K, fasudil hydrochloride couldn’t protect myocardial ischemia/reperfusion injury, the levels of apoptosis index and myocardial infarct size in the fasudil hydrochloride and an inhibitor of PI3K group were significantly higher than in the fasudil hydrochloride group （all P〈0.01）. Conclusion PI3K-Akt pathway was thought to be one of the main mechanisms responsible for the protection of fasudil hydrochloride postconditioning.

关 键 词：盐酸法舒地尔 药物后适应 缺血 再灌注 大鼠 

分 类 号：R363[医药卫生—病理学]