碘化正丁基氟哌啶醇对兔心肌缺血再灌注损伤血流动力学和心肌组织中酶的影响

目的　评价碘化正丁基氟哌啶醇 (N n butylhaloperi doliodide ,F2 )对心肌缺血再灌注损伤的保护作用 ,并探讨其作用机制。方法　结扎兔冠状动脉左室支 ,制成急性心肌缺血再灌注损伤模型 ,缺血前 5min ,静脉推注F2 ,观察在急性缺血和再灌注状态下血流动力学的变化及再灌注后心肌组织中超氧化物歧化酶 (SOD)、丙二醛 (MDA)、肌酸激酶(CK)、ATP酶的变化。结果　F2能剂量依赖地改善兔心肌缺血再灌注后的血流动力学变化 ,MAP、LVSP、±dp/dtmax均较缺血再灌注对照组升高 ,LVEDP有所降低 ;还能剂量依赖性地降低MDA的产生 ,保护心肌组织SOD的活性和Ca2 + ATPase、Na+ ,K+ ATPase的活性 ,保护心肌酶CK的释放。结论　F2对心肌缺血再灌注损伤有保护作用。

Effects of N-n-butyl haloperidol iodide on the hemodynamics and enzymes of myocardial tissue of myocardial ischemia-reperfusion injury in rabbits

AIM To evaluate the protective effect of N -n-butyl haloperidol iodide (F2) on myocardial ischemia-reperfusion injury, and to try to find the protective mechanism of F2. METHODS The myocardial ischemia-reperfusion injury animal model was established by ligaturing rabbit's left ventricular branch of coronary artery for 40 min and removing the ligationg later to reperfuse for 40 min in vivo . Different doses of F2 were administered by intravenous injection prior to the onset of ischemia. The changes of hemodynamics were recorded during the experiment, while those of superoxide dismutase (SOD), creatine kinase (CK), ATPase and the contents of malondiadehyde (MDA) of myocardial tissue were detected after reperfusion. RESULTS F2 could ameliorate the hemodynamics of ischemia-repefusion injured myocardium in a dose-dependent manner. The values of MAP, LVSP, ±d p /d t _ max were obviously higher than those of the ischemia-repefusion control group, while those of LVEDP were lower. F2 could also reduce the yield of MDA, protect the activities of SOD, Ca 2+ -ATPase, Na +,K +-ATPase, and minify the leakage of CK out of myocardial cells in a dose-dependent manner. CONCLUSION F2 could exert an apparently protective effect against myocardial ischemia-reperfusion injury.