碘化N-正丁基氟哌啶醇对大鼠心脏缺血和再灌注室性心律失常的拮抗作用  

Effects of N-n-butyl haloperidol iodide on ischemia and reperfusion-induced ventricular arrhythmias in rat heart

作　　者：高分飞[1] 石刚刚[1] 李海青[1] 黄展勤[1] 张艳美[1] 周燕琼[1] 

机构地区：[1]汕头大学医学院药理学教研室

出　　处：《中国临床药理学与治疗学》2007年第9期1004-1008,共5页Chinese Journal of Clinical Pharmacology and Therapeutics

基　　金：国家自然科学基金项目(30672465);广东省自然科学基金重点项目(06118928);面上项目(07008206);汕头市重点科技计划项目(2006)

摘　　要：目的:研究碘化N-正丁基氟哌啶醇(F2)对心肌缺血和再灌注引发的室性心律失常的拮抗作用。方法:采用大鼠Langendorff灌流心脏模型,通过结扎左冠脉前降支缺血20min,解除结扎再灌注,引出室性心律失常。缺血前5min用含不同浓度F2的台氏液灌流,观察其对缺血和再灌注期室性心律失常发生率的影响,同时观察F2对心电图上PR、QT、RR间期的影响。用心房起搏(5Hz)防止心率变慢,观察1μmol/LF2对缺血和再灌注室性心律失常、PR间期的影响。结果:F2可浓度依赖地降低缺血和再灌注期室性心律失常发生率,并减慢心率,延长PR间期。在心房起搏控制心律下,仍具有拮抗缺血和再灌注室性心律失常、延长PR间期的作用。结论:F2对大鼠心脏缺血和再灌注性心律失常具有直接的抑制作用。AIM：To study the antiarrhythmic effects of N-n-butyl haloperidol iodide（F2）on ischemia-and reperfusion-induced ventricular arrhythmias.METHODS：Using the Langendorff-perfused rat heart model,the ventricular arrhythmias were induced by ligating the left anterior descending coronary artery for 20 minutes before the release of the ligature.Each concentration of F2 was administered 5 min prior to the induction of regional ischemia.The effects of F2 on arrhythmias during periods of ischemia and reperfusion and the effects on PR,QT,RR intervals were investigated.When rat hearts were paced（5 Hz） via the right atrium to prevent bradycardia,the antiarrhythmic effects and the effect on PR interval of 1 μmol/L F2 were observed.RESULTS：F2 reduced ischemia-and reperfusion-induced ventricular arrhythmias in concentration-dependent manner,and widened PR,RR intervals.The same effects were observed even in paced rat hearts.CONCLUSION：F2 could reduce ischemia-and reperfusion-induced ventricular arrhythmias directly in the isolated rat hearts.

关 键 词：碘化N-正丁基氟哌啶醇 心律失常 缺血再灌注 

分 类 号：R971.4[医药卫生—药品]