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The vagus nerve modulates electrical activity of the cardiac ventricles. However, whether the vagus nerve mediates these effects through the conduction system or directly on the myocardium is unknown. Accordingly, we studied vagus nerve stimulation (VNS) during sinus rhythm and during ventricular fibrillation (VF) in porcine and ovine preparations. We sought to determine: 1) what is the most potent frequency with which to stimulate the vagus nerve and 2) whether VNS at that frequency produces any change in cardiac wall motion during ventricular fibrillation. We studied 8 pigs and 10 sheep that were anesthetized with urethane 1 mg/kg intravenously and placed on a ventilator. Platinum vagus nerve electrodes were wrapped around the nerves. Simultaneous electrocardiogram (EKG) and carotid artery blood pressure (BP) recordings were made. VNS was performed in animals with 1-millisecond pulses for 20 seconds at 1, 2, 5, 10, 20, 50, and 100 Hz. This was done on both vagus nerves separately and bilaterally. Potency of the VNS was evaluated by counting the number of beats within the 20 seconds. VF was produced in 4 pigs by opening the thorax and applying direct current to the ventricles. Epicardial echocardiography during VF was performed, and both vagus nerves were stimulated at 50 Hz for 20 seconds. Wall motion data was extracted during VF for three periods--before, during, and after VNS. All data are presented as means with S.E.M. and were compared using repeated measures ANOVA, and p-values are reported. Tukey post-hoc analysis was performed, and statistical significance was taken as p-values < 0.05. In both sheep and pigs, 50 Hz was found to be the optimal frequency required to produce cardiac standstill. Bilateral VNS in pigs at 20, 50, and 100 Hz produced 21 ± 13, 1 ± 1, and 24 ± 14 beats in 20 seconds of stimulation, respectively (p = 0.003, 50 Hz was significantly different from 20 and 100 Hz). Bilateral VNS in sheep at 20, 50, and 100 Hz produced 14 ± 6, 2 ± 2, and 18 ± 7 beats in 20 seconds of stimulation, respectively (p = 0.002, 50 Hz was significantly different from 20 and 100 Hz). Wall motion data during VF showed 0.065 ± 0.005, 0.030 ± 0.008, and 0.057 ± 0.004 centimeters mean displacement before, during, and after VNS, respectively (p = 0.005, wall motion during VNS was significantly smaller than the other groups). We conclude that 50 Hz is the optimal frequency for VNS to exert its optimal cardiac effects. Vagus nerve stimulation affects the ventricles in large animals in both sinus rhythm and VF. These findings suggest VNS may provide an alternative adjunct therapy to treat ventricular arrhythmias. [ABSTRACT FROM AUTHOR]

The recurrent laryngeal nerve (RLN) is a branch of the vagus nerve that controls the movement of the vocal folds and arytenoid cartilages. Since it is damaged in 4-10% of thyroid surgeries, a better characterization of its function may aid in finding ways to repair the consequent vocal fold paralysis after damage. To this end, we developed methods to measure RLN function and vocal fold movement in rats under normal conditions, after nerve crush or cut, and upon RLN stimulation in rats. Rats were anesthetized with urethane 1.5 mg/kg intraperitoneally. Right RLN activity was recorded, along with electrical activity of the posterior crico-arytenoid and thyro-arytenoid muscles. A microsuspension laryngoscope was fashioned to visualize the arytenoid cartilages, and the deviation of the cartilages from the midline on video served as a quantitative measure of vocal fold function. Breathing was assessed by recording changes in resistance over a piece of conductive rubber wrapped around the thorax. Recordings from the above techniques were taken simultaneously during normal vocal fold function and after nerve crush or cut. Average waveforms of a single respiratory cycle during normal function and after nerve injury were calculated for each recording. The RLN was stimulated at 1, 2, 5, 10, 20, and 50 Hz with 1-millisecond pulses under normal and nerve injury conditions. A total of 31 adult rats were used in these experiments. Under normal conditions, we found rhythmic firing in the RLN that correlated in time with electromyogram (EMG) activity, vocal fold movement, and breathing. Cutting or crushing the right RLN resulted in normal breathing, but cessation of RLN and EMG activity, as well as paralysis of the ipsilateral arytenoid near the midline position. Stimulation of the distal RLN under normal and cut conditions caused arytenoid twitches that occurred upon each pulse in the 1-10 Hz range. At 20 or 50 Hz, the arytenoid moved to or stayed at the midline during stimulation. The development of quantitative techniques to study RLN function is an important step towards validating a rat model for RLN lesions. Normal RLN activity causes opening and closing of the arytenoids, but overstimulation of the RLN may overpower the adductor muscles and cause midline paralysis of the vocal folds. Our results have implications for the study of RLN regeneration after injury, as nerve impulses occurring after re-innervation may be similar to indiscriminate RLN stimulation. [ABSTRACT FROM AUTHOR]