Transcutaneous auricular vagus nerve stimulation reduces ventricular arrhythmias and its mechanism

Abstract

Objective To investigate the effects and its possible mechanism of transcutaneous auricular vagus nerve stimulation (AB-VNS) on ventricular arrhythmias induced by myocardial infarction (MI) . Methods Fourteen healthy adult beagle dogs were randomly divided into two groups: AB-VNS group (ligate coronary artery +intermittent AB-VNS) and control group (ligate coronary artery but no AB-VNS) . We compared the incidence of ventricular arrhythmias (VA) , ventricular effective refractory period (VERP) , left ventricular function and histopathological changes between the two groups, and measured the distribution of vagus and sympathetic nerves and the protein expression of receptor in ventricular myocytes. Results ① Four weeks after AB-VNS, the premature ventricular contraction (PVCs) in 24 hours was significantly less than that in the control group (4 492 vs.5 593, P<0.05) . Non-sustained ventricular tachycardia was also less than that in the control group (174 vs. 256, P<0.05) . ②At 30 minutes after acute myocardial infarction (AMI) , the VERP was significantly shorter than the baseline level in epicardial 3, endocardium 1 and endocardium 2 sites (P<0.05) . Four weeks after AB-VNS, the VERP in the above 3 sites were significantly prolonged, compared with the baseline level and value 30 minutes after AMI in the AB-VNS group (P<0.05) .Thirteen minutes after AMI, the dispersion of ERP (dERP) was significantly increased compared with the baseline level in both groups.Four weeks after AB-VNS, the dERP was significantly decreased than that in the control group (P<0.05) . Four weeks after AB-VNS, the ventricular fibrillation threshold (VFT) in the AB-VNS group was significantly enhanced, compared with that in the control group (P<0.05) . ③Four weeks after AB-VNS, the nerve density of the left ventricular tyrosine hydroxylase (TH, 9674 μm/mm2 vs. 2 602 μm/mm2, P<0.05) and choline acetyl esterase (CHAT, 1 025 μm/mm2 vs. 2 950 μm/mm2, P<0.05) in the AB-VNS group were significantly lower than that in the control group. ④Four weeks after AB-VNS, the protein expression of adrenergic receptor β1、nerve growth factor P75 receptors and TrkA in peri-infarcted and non infarcted areas of left ventricular in the AB-VNS group were significantly lower than that in the control group (P<0.05) . Conclusion AB-VNS can inhibit the ventricular arrhythmias induced by MI, prolong the VERP and decrease the dERP, modulate the vagal/sympathetic imbalance, reverses sympathetic regeneration and improves the abnormal distribution of adrenergic receptors after MI, which may be the mechanism of AB-VNS in preventing VA after MI. Key words: Vagus nerve; Sympathetic nerve; Auricular branch; Myocardial infarction