奎尼丁所致异常U波与早期后除极的相关性研究

The Relative Investigation Between Abnormal U Wave and Early Afterdepolarization Induced by Quinidine

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。

To investigate the relationship between early afterdepolarization (EAD) and abnormal U wave ,the monophasic action potential(MAP)was recorded by endocardial contact electrode in 11 anesthetized dogs with quinidine-induced long QT syndrome. Large U wave showed a significant correlation with the amplitude of EAD(r=0.98,P<0.01),its peak time was synchronous,Both U wave and EAD were paused-dependent.The QTU interval increased from 240±19 to 415±74ms, MAPD90 from 223±18 to 348±82ms,and QTU interval showed a significant correlation with MAPD90(r=0.98,P<0.01).In one dog,bigeminal ventricular beat arose from neighboring region of the peak of EAD.The results suggested that the MAP technique should be a reliable method in studying the mechanisms of anti-arrhythmic drugs in viva and the relation between U wave and EAD.