• Xiaoya Zhou, Liping Zhou, Songyun Wang, Lilei Yu, Zhuo Wang, Bing Huang, Mingxian Chen, Jun Wan, and Hong Jiang.
• Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei, China.
• J. Cardiovasc. Electrophysiol. 2016 Feb 1; 27 (2): 217-23.

BackgroundHyperactivity of the cardiac sympathetic nervous system may underlie the pathogenesis of inappropriate sinus tachycardia (IST). Studies have proven that cervical vagal stimulation could inhibit stellate ganglion neural activity.SubjectsTo investigate whether noninvasive vagal nerve stimulation (NVNS) could inhibit sympathetically induced sinus node acceleration by reducing right stellate ganglion (RSG) neural activity.MethodsSixteen anesthetized dogs were randomly divided into NVNS group (with NVNS, n = 8) and control group (with sham NVNS, n = 8). NVNS was delivered to the vagus nerve innervating at the right tragus with a voltage of 80% below the threshold, the minimal voltage to slow the sinus rate or atrioventricular conduction. The maximal sinus rate accelerations induced by high-frequency stimulation (HFS) of RSG and RSG neural activity were measured at baseline and 3 hours after NVNS. At the end, SK2, c-fos, and NGF protein expression in RSG were examined in both groups.ResultsCompared to baseline, the maximal sinus node acceleration induced by RSG stimulation and the RSG neural activity were both significantly attenuated after 3 hours of NVNS (P < 0.05 for both). However, these indices did not change significantly in the control group (P > 0.05). SK2 expression in RSG was significantly higher and c-fos and NGF expressions were significantly lower in the NVNS group than those in the control group (P < 0.05).ConclusionNoninvasive vagal nerve stimulation may suppress RSG activity possibly by modulating SK2, c-fos, and NGF expressions in RSG, thus inhibiting sympathetically induced sinus node acceleration.© 2015 Wiley Periodicals, Inc.

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