Low-Level Right Vagal Stimulation: Anticholinergic and Antiadrenergic Effects

• Published in: Journal of cardiovascular electrophysiology 2011-10, Vol.22 (10), p.1147-1153
• Main Authors: SHA, YONG, SCHERLAG, BENJAMIN J., YU, LILEI, SHENG, XIA, JACKMAN, WARREN M., LAZZARA, RALPH, PO, SUNNY S.
• Format: Article
• Language: English
• Subjects: Adrenergic Fibers; Animals; atrial fibrillation; Atrial Fibrillation - etiology; Atrial Fibrillation - physiopathology; Atrial Fibrillation - prevention & control; autonomic ganglion; Cardiac Pacing, Artificial; Cholinergic Fibers; Disease Models, Animal; Dogs; Electric Stimulation; Electrophysiologic Techniques, Cardiac; Ganglia, Autonomic - physiopathology; Heart Atria - innervation; pulmonary vein; Pulmonary Veins - innervation; Time Factors; vagus; Vagus Nerve Stimulation
• ISSN: 1045-3873; 1540-8167
• DOI: 10.1111/j.1540-8167.2011.02070.x

Right Vagal Stimulation Suppresses Atrial Fibrillation. Introduction: We sought to extend the use of low‐level vagal stimulation by applying it only to the right vagus nerve (LL‐RVS) to suppress atrial fibrillation (AF). Methods: In 10 pentobarbital anesthetized dogs, LL‐RVS (20 Hz, 0.1 ms pulse width) was delivered to the right vagal trunk via wire electrodes at voltages 50% below that which slowed the sinus rate (SR) or atrio‐ventricular conduction. Electrode catheters were sutured at multiple atrial and pulmonary vein (PV) sites to record electrograms. LL‐RVS continued for 3 hours. At the end of each hour, 40 ms of high‐frequency stimulation (HFS; 100 Hz, 0.01 ms pulse width) was delivered 2 ms after atrial pacing (during the refractory period) to determine the AF threshold (AF‐TH) at each site. Other electrodes were attached to the superior left ganglionated plexi (SLGP) and right stellate ganglion (RSG) so that HFS (20 Hz, 0.1 ms pulse width) to these sites induced SR slowing and acceleration, respectively. Microelectrodes inserted into the anterior right ganglionated plexi (ARGP) recorded neural activity. Results: (1) Three hours of LL‐RVS induced a progressive increase in AF‐TH at all sites (all P < 0.05). (2) The SR slowing and acceleration response induced by SLGP and RSG stimulation, respectively, was blunted by LL‐RVS. (3) The frequency and amplitude of the neural activity recorded from the ARGP were markedly inhibited by LL‐RVS. Conclusions: LL‐RVS suppressed AF inducibility and the chronotropic responses to parasympathetic and sympathetic stimulation. Inhibition of neural activity in the GP may be a mechanism underlying these results. (J Cardiovasc Electrophysiol, Vol. 22, pp. 1147‐1153, October 2011)