目的:探讨特效转复心房颤动药物伊布利特致尖端扭转性室性心动过速(Tdp)的机制。方法:利用兔左室楔形心肌块灌流伊布利特或溶有伊布利特的低钾低镁台氏液。30只新西兰大白兔随机分为正常组、伊布利特组和低钾低镁组,每组10只。正常组灌流台氏液,伊布利特组灌流2 mg/L伊布利特40 min,低钾低镁组灌流同浓度但溶于低钾低镁台氏液的伊布利特。同步记录各组内、外膜下心肌动作电位和容积心电图,观察灌流过程中早后除极(EAD)和Tdp的发生情况,对QT间期以及跨室壁复极离散度(TDR)的影响。结果:伊布利特组QT间期较正常组显著延长[(337±46)ms∶(548±73)ms],TDR也显著增加[(49±15)ms∶(132±36)ms],EAD的发生率为4/10,与正常组比较,均P〈0.05;Tdp的发生率为0。低钾低镁组QT间期近一步延长至(652±184)ms、TDR增至(157±59)ms,EAD发生率为5/10,与正常组比较,均P〈0.05,与伊布利特组比较,均P〉0.05;Tdp的发生率增加为7/10,与正常组、伊布利特组比较,均P〈0.05。结论:在伊布利特合并低钾低镁的情况下才易诱发Tdp,电解质正常时不易致心律失常发生。
Objective:Ibutilide is a miracle drug to convert aterial fibrillation.The aim of this study is to discuss the mechanism of torsades de pointes(Tdp) induced by ibutilide in special condition.Method:Thirty artily rabbit left ventricular wedge preparations were randomly divided into control group(perfused with tyrode's solution),ibutilde group(perfused with 2 mg/L ibulitide),hypopotassemia and hypomagnesemia group(perfused with 2 mg/L ibulitide and hypopotassemia and hypomagnesemia tyrode's solution,10 preparations each).Transmural ECG and action potentials from both endocardium and epicardium were simultaneously recorded.The changes of QT interval,TDR,EAD,R on T extrasystole and Tdp were also analyzed.Result:Compared to control group,the QT interval and the TDR were increased in ibutilde group([548±73]ms vs [337±46]ms,[132±36]ms vs ms,all P〈0.05).The incidence of EAD in ibutilde group was also higher than it in control group(0/10 vs 4/10,P〈0.05).There was no significant difference in the incidence of Tdp between these two groups.The QT interval,TDR and the incidence of Tdp were further prolonged in hypopotassemia and hypomagnesemia group(all P〈0.05).Conclusion:Ibutilde can induce Tdp in the condition of hypopotassemia and hypomagnesemia,but can't induce Tdp in normal condition easily.