去自主神经条件下迷走神经对肺静脉不同部位房颤诱发率的影响

目的 探讨去自主神经条件下迷走神经对肺静脉不同部位房颤诱发率的影响。方法 10只健康杂种犬,经切断双侧颈迷走神经干和破坏颈交感神经节,建立动物的去自主神经模型。分别在右心耳、左心耳、左心房和四支肺静脉的近、中、远段行S1S1及S1S2程序刺激,在基础刺激及伴有双侧颈迷走神经同时刺激或阿托品作用的情况下,观察心房及肺静脉不同部位房颤诱发率的变化。结果 基础状态下,在心房及肺静脉的所有部位给予S1S2程序刺激,几乎均可诱发出房性早搏或短阵房速,而较少诱发出房颤。当同时伴有迷走神经刺激时,房颤的诱发频率明显增加;当行S1S1刺激的同时伴有双侧颈迷走神经刺激时,在心房及肺静脉的所有部位,其房颤诱发率均较基础刺激时明显升高（右心耳22．2％vs59．3％,左心耳14．8％vs55．6％,左心房18．5％vs51．9％,左上肺静脉上段33．3％vs66．7％,P〈0．05,P〈0．01）。与基础刺激比较,阿托品作用并不影响肺静脉的房颤诱发率（均P〉0．05）。结论 对于肺静脉起源的房颤,迷走神经也可能是参与其起始的重要诱发因素。

Vagal effects on inducibility of atrial fibrillation at different sites of pulmonary veins after autonomic denervation

Objective To investigate the vagal effects on the inducibility of atrial fibrillation (AF) at different sites of pulmonary vein after autonomic denervation. Methods The bilateral cervical vagal trunks of 10 male mongrel dogs were isolated and decentralized. The ansae subclaviae were exposed, ligated, and cut. Needle electrodes were inserted into the subcutaneous tissue of the 4 extremities to record the myocardiogram. Right ventricle electrode was introcuded via femoral vein and an electrode with 4 poles was sutured with the right appendage (RAA), left appendage (LAA), left atrium (LA), left superior pulmonary vein (LSPV), right superior pulmonary vein (RSPV), left inferior pulmonary vein(LIPV), and right inferior pulmonary vein(RIPV)respectively. Local burst stimulation (S1S1=80 ms, impulse duration=0.5 ms) was performed on these sites to record the baseline AF inducibility. When sinus cardiac arrest for 2 s or complete atrio-ventricular block occurred programmed bilateral vagal nerves stimulation (VNS) was performed with the frequency of 12.5 Hz, impulse duration of 0.5 ms, and voltage of 5~8 V. Atropine 0.04 mg/kg was dripped intravenously. The changes of AV inducibility were observed. Results In the baseline state, S1S1 programmed stimulation on all the sites evoked single or multiple atrial premature beats and short runs of atrial tachycardia, only a few sites induced AF. However, S1S1 programmed stimulation combined with VNS significantly increased the frequencies of induced AV at the sites of 4 PVs (P<0.05, P< 0.01). When atropine was dripped the AV induction rates at all sites did not changed significantly (all P> 0.05). Conclusion Vagal nerve may play an important role in the initiation of AF originating from pulmonary veins.