Loeb J M, Euler D E, Randall W C, Moran J F, Brynjolfsson G
Circulation. 1980 Jan;61(1):192-8. doi: 10.1161/01.cir.61.1.192.
Embolization of the sinus node artery was accomplished in dogs by injecting rapidly hardening vinyl latex into the sinus node artery. Embolization immediately shifted the pacemaker to a junctional focus; however, with time postoperatively, the pacemaker shifted to an atrial site. Variable episodes of pacemaker failure, sinoatrial block, junctional rhythm, wandering atrial pacemaker and idioventricular escape rhythms were commonly observed on Holter monitor in isolation but only rarely when the dog was in the laboratory. Severe bradycardia (38.9 +/- 3.7 beats/min) was the predominant rhythm by 3-6 months postoperatively. In addition, these same dogs had a greater overall increase in heart rate after atropine than normal dogs (17.5 +/- 13.5 vs 116.6 +/- 15.9 beats/min above control; p less than 0.02). Responses to vagal stimulation in this group were abnormal, as long periods of asystole and bradycardia were observed after stimulation was terminated. These data suggest an alteration in parasympathetic pacemaker control after chronic embolization of the sinus node artery.
通过将快速硬化的乙烯基乳胶注入犬的窦房结动脉来实现窦房结动脉的栓塞。栓塞立即将起搏点转移至交界性起搏点;然而,术后随着时间推移,起搏点转移至心房部位。在动态心电图监测中,常见到孤立的起搏器功能障碍、窦房阻滞、交界性心律、游走性心房起搏点及心室自主逸搏心律发作,但犬在实验室时很少出现。术后3至6个月,严重心动过缓(38.9±3.7次/分钟)成为主要节律。此外,这些犬在使用阿托品后心率的总体增幅大于正常犬(比对照组高17.5±13.5次/分钟与116.6±15.9次/分钟;p<0.02)。该组对迷走神经刺激的反应异常,在刺激终止后观察到长时间的心搏停止和心动过缓。这些数据提示,窦房结动脉长期栓塞后副交感神经对起搏点的控制发生了改变。