目的 观察法舒地尔对兔心肌缺血再灌注损伤的作用,并探讨其作用机制.方法 将36只新西兰大白兔按随机数字表法分成假手术组(Sham组)、缺血再灌注组(I/R组)、法舒地尔治疗组(F组),每组12只.建立兔急性MIRI模型,术中观察心电图变化,测定各组不同时间点血清肌酸激酶同工酶(CK-MB)、肌钙蛋白Ⅰ(cTnⅠ)、肿瘤坏死因子-α(TNF-α)和一氧化氮(NO)的含量;各组再灌注末取兔心肌组织在光学显微镜下观察其形态学变化,电境下观察其超微结构变化.结果 与I/R组相比,F组CK-MB、cTnⅠ、TNF-α的水平明显降低(P＜0.05),NO生成增加(P＜0.05);心肌组织形态学及超微结构损伤F组较I/R组明显减轻.结论 法舒地尔对兔缺血再灌注损伤心肌具有保护作用,并能明显减轻心肌细胞和组织的损伤.其机制可能与法舒地尔的抗炎及保护血管内皮功能有关.%Objective To study the protective effect of fasudil on myocardial ischemia-reperfu-sion injury (MIRI) in rabbits and its mechanism of action. Methods Thirty-six New Zealand rabbits were randomly divided into three groups: sham operation group (Sham group) , ischemia-reperfusion group (I/R group) and fasudil treatment group (F group), with 12 rabbits in each group. The model of acute MIRI was established. Intraoperative electrocardiogram changes were observed and levels of serum creatine kinase MB(CK-MB) , troponin I (cTn I ) , tumor necrosis factor-α(TNF-α)and nitric oxide(NO) were detected at different time points. At the end of reper-fusion,the morphological changes in myocardial tissue were observed under an optical microscope and the ultrastructural changes were observed with an electron microscope. Results Compared with I/R group, CK-MB, cTn I and TNF-α levels and structural damage significantly decreased and NO levels obviously increased in F group(P<0. 05). Conclusion Fasudil exerts a protective effect on MIRI and reduces myocardial cell and tissue damage through a mechanism involving anti-inflammation and vascular protection.
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