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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。
The epicardial monophasic action potential (MAP) of rabbits was recorded. CsX was used to establish the model of polymorphic ventricular tachycardia (VT) , To study the inhibitory effect of Cromakalim on triggering activity and TdP. The results showed that: (1) EEC and ventricular arrhythmia occurred in 16 rabbits (10 of them were TdP) after CsCl administration. The onset potential of ectopic ventricular beats, the coupling duration and the amplitude of EAD were highly correlated with the coupling duration (r = 0.94, 0.97, respectively); (2) Compared with pre-treatment, The incidence of EAD decreased (100% vs18.8%, P <0.05), and the average amplitude decreased (11.5 ± 2.6mVVS5.2 ± 4.0mV, P <0.05) Lin can correct CsCl caused by a variety of ventricular arrhythmias. The results suggest that: (1) Triggering activity is an important mechanism of TdP in long QT interval; (2) Chloramphenicol has a therapeutic effect on long QT interval TdP through inhibition of triggering activity.