Schuessler R B, Rosenshtraukh L V, Boineau J P, Bromberg B I, Cox J L
Department of Surgery, Washington University School of Medicine, Barnes Hospital, St. Louis, Mo. 63110.
Circ Res. 1991 Oct;69(4):1075-87. doi: 10.1161/01.res.69.4.1075.
Atrial fibrillation occurs spontaneously after bradycardia induced by acetylcholine infusion or vagal stimulation. To determine the mechanism of initiation of this tachyarrhythmia, we infused acetylcholine (5 ml, 10(-3.5) M) into Krebs-Henseleit-perfused isolated canine right atria (n = 10). Unipolar electrograms were recorded from 250 sites simultaneously during control rhythms, pacing (cycle length = 300 msec) with and without acetylcholine, and recovery of spontaneous activity. Activation sequence maps were constructed from each recording. Stable spontaneous rhythm was present in all preparations during control conditions. Activation sequence maps, recorded during continuous pacing with and without acetylcholine, demonstrated no dromotropic changes due to the acetylcholine. Focal asynchronous recovery of spontaneous activity was initiated from different sites, resulting in bigeminal or trigeminal premature depolarizations in 41 of 73 cases after infusion of acetylcholine. A reentrant tachyarrhythmia was initiated in 24 of 41 cases by the closely coupled recovery beats (A1A2 = 100 +/- 37 msec; A2A3 = 97 +/- 27 msec). The reentry was initiated by interaction of the premature impulse with regions of functional block that were a result of the cholinergically induced dispersion of refractoriness. All the tachyarrhythmias terminated spontaneously, and stable spontaneous control rhythms returned. In conclusion, the data suggest that the premature depolarizations that initiate the reentrant tachyarrhythmia are caused by the asynchronous recovery of multiple right atrial pacemakers accompanied by variable entrance block at the later depolarizing sites.
在通过输注乙酰胆碱或迷走神经刺激诱导心动过缓后，心房颤动会自发发生。为了确定这种快速性心律失常的起始机制，我们将乙酰胆碱（5毫升，10^(-3.5) 摩尔/升）注入用Krebs-Henseleit溶液灌注的离体犬右心房（n = 10）。在对照节律、有和没有乙酰胆碱的起搏（周期长度 = 300毫秒）以及自发活动恢复期间，同时从250个部位记录单极电图。根据每次记录构建激动顺序图。在对照条件下，所有标本均存在稳定的自发节律。在有和没有乙酰胆碱的持续起搏期间记录的激动顺序图显示，乙酰胆碱未引起传导性改变。自发活动从不同部位开始局灶性异步恢复，导致在注入乙酰胆碱后的73例中有41例出现二联律或三联律早搏。在41例中的24例中，由紧密耦合的恢复搏动引发了折返性快速性心律失常（A1A2 = 100 +/- 37毫秒；A2A3 = 97 +/- 27毫秒）。折返是由过早冲动与功能性阻滞区域相互作用引发的，功能性阻滞区域是由胆碱能诱导的不应期离散导致的。所有快速性心律失常均自发终止，稳定的自发对照节律恢复。总之，数据表明，引发折返性快速性心律失常的早搏是由多个右心房起搏器的异步恢复以及后期去极化部位的可变入口阻滞引起的。
