肺静脉起源的局灶性心房颤动模型：心房颤动触发机制与维持机制的分离

目的建立非肺静脉起源的局灶性心房颤动（房颤）模型,观察该房颤的诱发和维持特点并探讨其可能的电生理机制。方法21只健康成年犬静脉麻醉后行右侧开胸手术,暴露靠近右上肺静脉的心脏脂肪垫（内含神经丛）,将1根多电极导管固定贴靠于右上肺静脉,使其头端电极贴靠右上肺静脉与左心房交界处,另外将2根多电极导管分别固定于右心房中部和右心耳一侧。用一根细塑料管固定于右心耳与右心房交界处,将二者隔离开,隔离出的右心耳面积大约为240mm2。另将一根单向动作电位（MAP）导管经股静脉送至右心耳内以记录局部的单向动作电位。其中6只犬在右房中部用胶水固定一塑料的中空圆柱体,其内部面积大约为8mm2。分别以不同浓度（1、10、100mmol/L）的乙酰胆碱（Ach）浸润分离出的右心耳和圆柱体内部的心房表面。结果21只犬中有16只犬应用100mmol/L Ach浸润右心耳可重复发生自发持续性局灶性房颤（〉10min）。右心耳处房颤的平均周长为30.6±4.6 ms,心房部位房颤的平均周长为105.2±32.0 ms（P〈0.05）。房颤发生前均伴有MAP时程〉90%的缩短。在房颤发作中,沿右心耳与右房交界处采用血管钳钳夹可导致全部16只犬右心耳处电活动的消失,但其中14只犬的房颤仍然在心房内持续存在,另2只犬的房颤在30 s内终止。6只犬在行右上肺静脉附近的神经丛内注射甲醛溶液后,再行100mmol/L Ach浸润右心耳仅造成MAP时程的明显缩短,不再能发生自发持续性房颤;全部6只犬Ach浸润圆柱体内部的心房表面不能发生自发持续性房颤。结论采用100mmol/L的Ach浸润足够面积的右心耳可建立右心耳起源的局灶性房颤模型。内源性自主神经系统在该房颤的触发和维持机制中起作用。

Spontaneous focal atrial fibrillation arising from a peripheral atrial site: separation of AF triggers from AF maintenance

Objective To produce an canine model of paroxysmal atrial fibrillation （AF） arising from a peripheral atrial site and to investigate the mechanism of the AF triggers and AF maintenance. Methods In 21 anesthetized dogs, the heart was exposed via right thoracotomy. Multi-electrode catheters were secured to the right superior pulmonary vein, mid portion of the right atrium （RA） and along a portion of the RA appendage （RAA）. A plastic tube was attached as a barrier to separate the RAA from the RA creating an area about 240 mm2. In addition, a monophasic action potential （MAP） was recorded from a catheter wedged in the RAA. In 6 dogs a cylinder was glued over a pair of electrodes on the RA creating a leak proof area （8 mm2）. Acetylcholine （Ach 1, 10, 100 mmol/L） was applied via a gauze patch on the RAA and in separate experiments instilled into the cylinder on the RA. Results 16 out of the 21 dogs only 100 mmol/L Ach applied to the RAA resulted in reproducible, spontaneous, sustained focal AF （ 〉 10 minutes）. The average cycle length （CL） at the RAA was 30. 6±4. 6 msec vs. 105.2 ±32. 0 msec at other atrial sites （ P 〈 0. 05 ）. AF was preceded by an ≥ 90% reduction of the MAP duration. Isolation by clamping across the RAA caused cessation of activity in this area but AF continued in 14 of the 16 dogs and AF stopped in the other 2 within 30 seconds. In 6 dogs, injection of formaldehyde into the GP at the entrance of the RSPV prevented spontaneous AF despite marked shortening of MAP due to Ach on the RAA. In another 6 dogs, instillation of 100 mmol/L Ach in the cylinder failed to induce AF. Conclusion Ach （100 mmol/L） applied over relatively large area of the RAA was sufficient to shorten refractoriness and trigger paroxysmal AF. Intrinsic cardiac autonomic system might participate in the mechanism of AF triggers and AF maintenance.