Transcutaneous Auricular Branch Of The Vagus Nerve Stimulation Reduces Ventricular Arrhythmias And Its Mechnism

Objective: To investigate the occurrence and mechanism of auricular branch of 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: a AB-VNS group(ligate coronary artery + intermittent AB-VNS)and a 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 the distribution of vagus and sympathetic nerves and the protein expression of receptor were measured in ventricular myocytes.Results:(1)In the AB-VNS group,the frequency of ventricular arrhythmia of 24 hours was significantly shorter than that in the control group after 4 weeks(P<0.05).(2)At 30 min after AMI,VERP was significantly shorter than baseline level in epicardial 3,endocardium 1 and endocardium 2 sites(P<0.05).In 4 weeks after AMI,VERP in the above 3 sites was significantly prolonged,Compared with the baseline level and the value at 30 min after AMI,In the AB-VNS group(P<0.05).At 30 min after AMI,the dispersion of ERP(dERP)was significantly prolonged,compared with the baseline level in the both groups.In 4 weeks after AMI,,dERP was significantly shorter than that in the control group(P<0.05).In 4 weeks after AMI,ventricular fibrillation threshold(VFT)in the AB-VNS group was significantly enhanced,comparared with that in the control group(P<0.05).(3)In 4 weeks after AMI,,the nerve density of tyrosine hydroxylase(TH)and choline acetyl esterase(CHAT)of left ventricles in the AB-VNS group were significantly lower than those in the control group(P<0.05).(4)In 4 weeks after AMI,protein expression of Adrenergic receptor ?1(ADRB1),Nerve growth factor(NGF)P75 and TrkA receptors in the infracted and non infarcted regions of left ventricular in the AB-VNS group were significantly lower than those in the control group,(P<0.05).Conclusions: AB-VNS can inhibit the occurrence of VA,prolong VERP and decrease DERP after MI.AB-VNS modulates 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.