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目的研究肺静脉电隔离(PVI)对犬的心房迷走神经功能及心房电重构的影响,以探讨PVI治疗心房颤动的可能机制。方法选取成年杂种犬18只,分为A组和B组。应用硫代巴比妥钠麻醉后分离并结扎双侧颈交感迷走神经干。静脉应用美托洛尔阻断交感神经活性。A组:9只犬,房间隔穿刺后,先行PVI,后以600次／min起搏右心房30 min,构建急性心房电重构模型。B组:9只犬,行房间隔穿刺后构建急性心房电重构模型。分别于PVI前后及心房电重构前后在基础状态及迷走神经刺激时测量右心耳(PAA)、左心耳(LAA)、冠状静脉窦近端(CSp)和冠状静脉窦远端(CSd)的不应期(ERP)、心房易感窗口(VW)及窦性周长(SCL)。结果①PVI对迷走神经的影响:A组犬PVI后迷走神经刺激对SCL影响较消融前明显降低(P<0．01)。PVI后迷走神经刺激对心房ERP的影响较消融前明显减弱(P<0．05)。PVI后迷走神经介导的心房颤动诱发率明显下降(P<0．05)。②PVI对心房电重构的影响:A组心房电重构后基础状态下和迷走神经刺激时测得的ERP较重构前无明显变化(P>0．05)。心房电重构前后基础及迷走神经刺激下均不能诱发心房颤动。B组心房电重构后基础状态下和迷走神经刺激时测得的ERP均明显缩短(尸值分别<0．01、0．05)。心房电重构前后基础状态下均不能诱发心房颤动,心房电重构后迷走神经刺激下的VW明显增宽(P<0．05)。B组电重构后基础状态和迷走神经刺激时的ERP缩短值较A组明显增加(P<0．05)。结论PVI可导致心房局部去神经反应,抑制迷走神经介导的心房颤动发生。心房电重构伴随着迷走神经对心房电生理特性调节活动增强,迷走神经介导的心房颤动易感窗口增宽。PVI能减轻心房电重构,其机制可能为心房去迷走神经效应。
Objective To investigate the effect of pulmonary vein isolation (PVI) on atrial vagal nerve function and atrial electrical remodeling in dogs to explore the possible mechanism of PVI in the treatment of atrial fibrillation. Methods 18 adult crossbred dogs were selected and divided into A group and B group. Bilateral neck cervical sympathetic vagus nerve was isolated and ligated after anesthesia with thiobarbituric sodium. Intravenous metoprolol blocks sympathetic activity. A group: 9 dogs, atrial septal puncture, the first PVI, after 600 beats / min pacing the right atrium for 30 min, the construction of acute atrial electrical remodeling model. Group B: Nine dogs, atrial septal puncture after the construction of acute atrial electrical remodeling model. The right atrial appendage (PAA), left atrial appendage (LAA), proximal coronary sinus (CSp) and distal coronary sinus (CSd) should be measured before and after PVI and before and after atrial electrical remodeling ERP, VW and SCL. Results ① The effect of PV on the vagus nerve: The vagus nerve stimulation after PVI in group A was significantly lower than that before ablation (P <0.01). The effect of vagal stimulation on atrial ERP after PVI was significantly weaker than that before ablation (P <0.05). Vagus nerve-mediated atrial fibrillation was significantly decreased after PVI (P <0.05). (2) The effect of PVI on atrial electrical remodeling: There was no significant change of ERP in basal atrial electrical remodeling and vagus nerve stimulation in group A before reconstruction (P> 0.05). Atrial electrical remodeling before and after basal and vagal stimulation can not induce atrial fibrillation. In the group B, the ERP measured at baseline and vagus nerve stimulation significantly shortened (p <0.01, 0.05 respectively). Atrial fibrillation was not induced in basal state before and after atrial electrical remodeling. VW was significantly increased after vagal stimulation in atrial electrical remodeling (P <0.05). Compared with group A, the basal state and the shortening of ERP in vagus nerve stimulation in group B were significantly increased (P <0.05). Conclusion PVI can cause local atrial denervation and inhibit vagal-mediated atrial fibrillation. Atrial electrical remodeling accompanied by vagal atrial electrophysiological properties of regulatory activity increased, vagal-mediated atrial fibrillation susceptibility window widened. PVI can reduce atrial electrical remodeling, the mechanism may be atrial vagal nerve effect.