Oliveira Mário, Silva M Nogueira, Geraldes Vera, Postolache Gabriela, Xavier Rita, Laranjo Sérgio, Rocha Isabel, Ferreira Rui, Silva-Carvalho Luís
Serviço de Cardiologia do Hospital de Santa Marta, Lisboa, Portugal.
Rev Port Cardiol. 2010 Mar;29(3):375-89.
Vagal activity is thought to influence atrial electrophysiological properties and play a role in the initiation and maintenance of atrial fibrillation (AF). In this study, we assessed the effects of acute vagal stimulation (vagus_stim) on atrial conduction times, atrial and pulmonary vein (PV) refractoriness, and vulnerability to induction of AF in the rabbit heart with intact autonomic innervation.
An open-chest epicardial approach was performed in 11 rabbits (New Zealand; 3.9-5.0 kg), anesthetized and artificially ventilated after neuromuscular blockade. A 3-lead ECG was obtained. Atrial electrograms were recorded along the atria, from right to left (four monopolar electrodes), together with a circular electrode adapted for proximal left PV assessment. Acute vagus nerve stimulation was obtained with bipolar electrodes (20 Hz). Epicardial activation was recorded in sinus rhythm, and the conduction time from right (RA) to left atrium (LA), and from RA to PVs, was measured in basal conditions and during vagus_stim. The atrial effective refractory period (ERP) and dispersion of refractoriness (Disp_A) were analyzed. Vulnerability to AF induction was assessed at the right (RAA) and left (LAA) atrial appendages and the PVs. Atrial stimulation (50 Hz) was performed alone or combined with vagus_stim. Heart rate and blood pressure were monitored.
In basal conditions, there was a significant delay in conduction from RA to PVs, not influenced by vagus_stim, and the PV ERPs were shorter than those measured in LA and LAA, but without significant differences compared to RA and RAA. During vagus_stim, conduction times between RA and LA increased from 16+8 ms to 27+6 ms (p < 0.05) and ERPs shortened significantly in RA, LAA and LA (p < 0.05), but not in RAA. There were no significant differences in Disp_A. AF induction was reproducible in 45% of cases at 50 Hz and in 100% at 50 Hz+vagus_stim (p < 0.05). The duration of inducible AF increased from 1.0 +/- 0.2 s to 12.0 +/- 4.5 s with 50 Hz+vagus_stim (p < 0.01). AF lasted >10 s in 45.4% of rabbits during vagus_stim, and ceased after vagus_stim in 4 out of these 5 cases. In 3 animals, PV tachycardia, with fibrillatory conduction, induced with 50 Hz PV pacing during vagus_stim.
Vagus_stim reduces interatrial conduction velocity and significantly shortens atrial ERP, contributing to the induction and duration of AF episodes in the in vivo rabbit heart. This model may be useful for the assessment of autonomic influence on the pathophysiology of AF,
迷走神经活动被认为会影响心房电生理特性，并在心房颤动（AF）的起始和维持中起作用。在本研究中，我们评估了急性迷走神经刺激（迷走神经刺激）对具有完整自主神经支配的兔心脏的心房传导时间、心房和肺静脉（PV）不应期以及房颤诱发易感性的影响。
对11只兔子（新西兰兔；3.9 - 5.0千克）进行开胸心外膜手术，在神经肌肉阻滞后进行麻醉并人工通气。记录三导联心电图。沿心房从右到左记录心房电图（四个单极电极），同时使用适合评估左肺静脉近端的环形电极。用双极电极（20赫兹）进行急性迷走神经刺激。在窦性心律下记录心外膜激动，并在基础状态和迷走神经刺激期间测量从右心房（RA）到左心房（LA）以及从RA到肺静脉的传导时间。分析心房有效不应期（ERP）和不应期离散度（Disp_A）。在右心房（RAA）和左心房（LAA）以及肺静脉处评估房颤诱发易感性。单独或联合迷走神经刺激进行心房刺激（50赫兹）。监测心率和血压。
在基础状态下，从RA到肺静脉的传导存在显著延迟，不受迷走神经刺激影响，肺静脉ERP比在LA和LAA中测得的短，但与RA和RAA相比无显著差异。在迷走神经刺激期间，RA和LA之间的传导时间从16 + 8毫秒增加到27 + 6毫秒（p < 0.05），RA、LAA和LA的ERP显著缩短（p < 0.05），但RAA中未缩短。Disp_A无显著差异。在50赫兹时，45%的病例可重复诱发房颤，在50赫兹 + 迷走神经刺激时100%可诱发（p < 0.05）。50赫兹 + 迷走神经刺激时，可诱发房颤的持续时间从1.0 ± 0.2秒增加到12.0 ± 4.5秒（p < 0.01）。在迷走神经刺激期间，45.4%的兔子房颤持续时间>10秒，在这5例中的4例中，迷走神经刺激停止后房颤终止。在3只动物中，在迷走神经刺激期间，5�赫兹肺静脉起搏诱发了伴有颤动传导的肺静脉心动过速。
迷走神经刺激降低心房间传导速度并显著缩短心房ERP，有助于体内兔心脏房颤发作的诱发和持续时间。该模型可能有助于评估自主神经对房颤病理生理学的影响。
