摘要
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.
关键词
单相动作电位
早期后除极
U波
心律失常
Monophasic action potential
Early afterdepolarization
U wave
Quinidine