SPONTANEOUS TACHYARRHYTHMIAS AFTER CHOLINERGIC SUPPRESSION IN THE ISOLATED PERFUSED CANINE RIGHT ATRIUM
SPONTANEOUS TACHYARRHYTHMIAS AFTER CHOLINERGIC SUPPRESSION IN THE ISOLATED PERFUSED CANINE RIGHT ATRIUM
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DOI：
10.1161/01.res.69.4.1075
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发表时间：
1991-10-01
影响因子：
20.1
通讯作者：
COX, JL
中科院分区：
文献类型：
--
作者：
SCHUESSLER, RB;ROSENSHTRAUKH, LV;COX, JL
心房颤动在乙酰胆碱输注或迷走神经刺激引起的心动过缓后自发发生。为了确定这种心动过速的起始机制，我们将乙酰胆碱（5 ml, 10(-35) M）注入krebs - henseleet灌注的离体犬右心房（n = 10）。在对照节律、使用和不使用乙酰胆碱的起搏（周期长度= 300 msec）和自发活动恢复期间，同时记录250个部位的单极电图。根据每个记录构建激活序列图。在控制条件下，所有制剂均有稳定的自发节律。在使用和不使用乙酰胆碱的连续起搏期间记录的激活序列图显示，乙酰胆碱没有引起促性改变。自发性活动的局部非同步恢复是从不同部位开始的，在输注乙酰胆碱后73例中有41例导致双叉或三叉神经过早去极化。41例患者中有24例由紧密耦合的恢复心跳（A1A2 = 100 +/- 37 msec; A2A3 = 97 +/- 27 msec）引发再入性速性心律失常。再入是由过早冲动与功能阻滞区域的相互作用引起的，这是胆碱能诱导的耐火性分散的结果。所有的快速心律失常都自动终止，稳定的自发控制节律恢复。综上所述，这些数据表明，导致再入性心动过速的过早去极化是由多个右心房起搏器的非同步恢复引起的，并伴有后去极化部位的可变入口阻滞。
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(-35) 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.