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用心外膜接触电极记录犬左室外膜单相动作电位（MAP），观察维拉帕米（异搏定）对氯化铯（CsCl）诱发的早期后除极（EADs）、QT间期延长及室性心动过速（VT）的影响。11只大，CsCl按0．5mg·kg-1次（首剂加倍），每15分钟一次静脉注射，直至诱发出VT。然后在给下一剂CsCl前，先给予维拉帕米0．1～0．2mg／kg静脉注射，后再给予此剂CsCl，以后仍每15分钟静脉注射CsCl一次直至VT再被诱发。结果维拉帕米给药前及给药后的15～60分钟CsCl诱发的EAD振幅占相应MAP振幅的29．2±7．0％和24．8±8．1％、QTc间期分别从对照组386±33ms延长至443±66ms（P＜0．01）和从441±107ms延长至516±93ms（P＜0．01），但给予维拉帕米后即刻，CsCl诱发的EADs仅为16．7±7．6％（与前述二值比较P均＜0．01）、QTc间期仅从对照的418±56ms延长至425±49ms（P＞0．05）。给维拉帕米前CsCl分别在7只和4只诱发出持续性和非持续性室速，给予维拉帕米后即刻仅在4只诱发出非持续性室速。结果示维拉帕米可以抑制CsCl诱发的EADS、QT间期延长及VT。
The left ventricular extracorporeal single-phase action potential (MAP) was recorded with the adventitial contact electrode and the effects of verapamil on CsCl-induced early post-depolarization (EADs) and QT prolongation Effects of ventricular tachycardia (VT). 11 large, CsCl 0.5mg · kg-1 times (the first dose doubled), intravenous injection every 15 minutes until VT evoked. Then before giving the next CsCl, verapamil 0.1 ~ 0.2mg / kg intravenous injection, and then given this agent CsCl, but still every 15 minutes intravenous injection of CsCl once until VT was induced. Results The CsCl-induced EAD amplitude before and after verapamil administration was 29.2 ± 7.0% and 24.8 ± 8.1% of the corresponding MAP amplitude at 15 to 60 minutes after administration, respectively. The QTc interval was The control group prolonged from 386 ± 33 ms to 443 ± 66 ms (P <0.01) and from 441 ± 107 ms to 516 ± 93 ms (P <0.01), but immediately after administration of verapamil, CsCl-induced EADs were only 16.7 ± 7.6% (P <0.01 compared with the above two values), QTc interval increased from 418 ± 56ms to 425 ± 49ms (P> 0.05) only from the control. CsCl at or before verapamil induced persistent and non-sustained VTs at 7 and 4, respectively. Only 4 of the CsCl administered verapamil induced non-sustained VT. The results showed that verapamil inhibited CsCl-induced EADS, QT interval prolongation and VT.