克罗卡林对长QT间期扭转型室性心动过速的治疗作用及机制

记录家兔心外膜单相动作电位（ＭＡＰ），应用氯化铯（ＣｓＣｌ）建立多形性室性心动过速（简称室速）模型，模拟临床ＱＴ间期延长扭转型室速（ＴｄＰ），研究克罗卡林（Ｃｒｏｍａｋａｌｉｍ）对触发活动及ＴｄＰ的抑制作用。结果显示：（１）应用ＣｓＣｌ后，１６只家兔均出现早期后除极（ＥＡＤ）及室性心律失常（其中１０只为ＴｄＰ）。异位心室搏动的启动电位、耦联间期与ＥＡＤ的振幅及耦联间期高度相关（ｒ分别为０．９４，０．９７）；（２）与用药前相比，克罗卡林使ＥＡＤ发生率下降（１００％ＶＳ１８．８％，Ｐ＜０．０５），平均振幅降低（１１．５±２．６ｍＶＶＳ５．２±４．０ｍＶ，Ｐ＜０．０５）；（３）克罗卡林能纠正ＣｓＣｌ引起的各种室性心律失常。结果提示：（１）触发活动为长ＱＴ间期ＴｄＰ的重要发生机制；（２）克罗卡林通过抑制触发活动而对长ＱＴ间期ＴｄＰ产生治疗作用。

Effect and Mechanism of Cromakalim on Torsades de Pointes With Long QT Interval

Through recording of the epicardial monophasic action potentials(MAP)with a contact electrode and using CsCl to induce polymorphous venrticular tachycardias,the effects of cromakalim on triggered activity and torsades de pointes(TdP)with long QT interval were investigated in rabbits in vivo.The findings showed that(1)CsCl induced early afterdepolarizations(EAD)and ventricular arrhythmias in all 16 rabbits,and 10 of them showed TdP with long QT interval.The take-off potentials and coupling intervals of premature ventricular beats(PVB )were strongly related to the amplitude and coupling intervals of EAD(r=0.94 and 0.97).(2 ) After the cromakalim infusion,the incidence of EAD reduced (100%VS 18.8%,P<0. 05) and the amplitude decreased (11.5± 2. 6 mV VS5.2±4.0mV,P<0.05).(3)Cromakalim eliminated all kinds of ventricular arrhythmias induced by CsCl. These data supports the conclusion that :(1)The triggered activty of EAD is an important mechanism of TDP with long QT interval.(2)The mechanism of cromakalim in eliminating TdP with long QT interval is through the supression of EAD.