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静脉注射中毒剂量奎尼丁建立ＱＴＵ间期延长综合征动物模型，应用接触电极导管记录犬左室心内膜单相动作电位（ＭＭ），以研究早期后除极（ＥＡＤ）与Ｕ波的关系。用药后１１条犬体表心电图上均出现异常Ｕ波，同步记录的ＭＡＰ３相上可见高振幅ＥＡＤ，二者振幅高度相关（ｒ＝０．９８），峰值时间基本一致。Ｕ波与ＥＡＤ均具有间歇依赖特性。用药后ＱＴＵ间期由对照的２４０±１９ｍｓ延长至４１５±７４ｍｓ，ＭＡＰ复极至９０％的时间（ＭＡＰＤ＿（９０））由对照的２２３±１８ｍｓ延长至３４８±８２ｍｓ，二者相关良好（ｒ＝０．９８）．用药后，１条犬发生频发成对室性早搏，呈“ＲｏｎＴＵ”现象。ＭＡＰ记录显示提前除极起源于ＥＡＤ峰值近处。无自发性尖端扭转型室性心动过速发生。研究结果表明：ＭＡＰ技术是研究在体心脏抗心律失常药物作用机理的可靠方法；体表心电图上异常Ｕ波可能来源于ＭＡＰ上的ＥＡＤ；ＭＡＰＤ９０是较ＱＴＵ间期更为精确的指标；奎尼丁诱发心律失常机制可能为触发活动。
Intravenous injection of poisoning dose quinidine to establish animal model of QTU prolongation syndrome, the application of contact electrode catheter recording canine ventricular endocardial monophasic action potential (MM) to study the relationship between early post-depolarization (EAD) and U waves . Abnormal U waves appeared on the surface electrocardiogram (ECG) of 11 dogs after treatment. High amplitude EAD was observed on the simultaneously recorded MAP3 phase. The amplitude of the two was highly correlated (r = 0.98), and the peak time was basically the same. U wave and EAD are intermittent dependent. After treatment, the QTU interval prolonged from 240 ± 19ms to 415 ± 74ms in the control group, prolonged from 223 ± 18ms in the control group to 348 ± 82ms in MAP repolarization to 90% (r = 0.98). After treatment, a dog frequent occurrence of premature ventricular contractions, was “RonTU” phenomenon. MAP records show that early depolarization originates near the peak EAD. No spontaneous torsades de pointes ventricular tachycardia occurred. The results show that MAP is a reliable method to study the mechanism of anti-arrhythmic drugs in vivo. The abnormal U wave on the surface ECG may originate from the EAD on MAP. MAPD90 is more accurate than the QTU interval. D-induced arrhythmia may be triggering activity.