Liu Peng, Guo Ji-hong, Zhang Hai-cheng, Sun Jian-ling, Yi Zhong, Liu Gang
Department of Clinical Electrophysiology, People's Hospital, Beijing University, Beijing 100044, China.
Zhonghua Yi Xue Za Zhi. 2006 Feb 7;86(5):317-20.
To investigate the vagal effects on the inducibility of atrial fibrillation (AF) at different sites of pulmonary vein after autonomic denervation.
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 introduced 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.
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).
Vagal nerve may play an important role in the initiation of AF originating from pulmonary veins.
探讨自主神经去支配后迷走神经对肺静脉不同部位房颤(AF)诱发率的影响。
选取10只雄性杂种犬,分离并离断双侧颈迷走神经干。暴露、结扎并切断锁骨下袢。将针电极插入四肢皮下组织记录心电图。经股静脉插入右心室电极,将四极电极分别缝于右心耳(RAA)、左心耳(LAA)、左心房(LA)、左上肺静脉(LSPV)、右上肺静脉(RSPV)、左下肺静脉(LIPV)和右下肺静脉(RIPV)。对这些部位进行局部猝发刺激(S1S1 = 80 ms,脉冲持续时间 = 0.5 ms)以记录基线房颤诱发率。当出现2 s窦性心脏停搏或完全性房室传导阻滞时,以12.5 Hz的频率、0.5 ms的脉冲持续时间和5 - 8 V的电压进行双侧迷走神经程控刺激(VNS)。静脉滴注0.04 mg/kg阿托品。观察房颤诱发率的变化。
在基线状态下,所有部位的S1S1程控刺激均诱发单个或多个房性早搏及短阵房性心动过速,仅少数部位诱发房颤。然而,S1S1程控刺激联合VNS显著增加了4条肺静脉部位的房颤诱发频率(P < 0.05,P < 0.01)。滴注阿托品后,所有部位的房颤诱发率均无明显变化(均P > 0.05)。
迷走神经可能在肺静脉起源的房颤起始中起重要作用。