Pulmonary Artery Denervation Reduces Ventricular Tachycardia From Right Ventricular Outflow Tract Induced By Left Stellate Ganglion Stimulation

Background:In recent years,more and more studies have shown that the autonomic nervous system plays an important role in the occurrence and development of ventricular arrhythmias.A large number of basic experiments and clinical studies have confirmed that autonomic imbalance based on sympathetic activation is closely related to ventricular arrhythmia originating from the right ventricular outflow tract(RVOT).Stimulation of the left stellate ganglion(LSG)facilitates the occurrence of ventricular arrhythmias from RVOT.Previous anatomical literatures have reported that the neural pathway originating from the LSG and the cervical ganglia reached the right ventricle after the pulmonary artery(PA).So we speculated that the pulmonary artery denervation(PADN)may reduce ventricular arrhythmias originating from the RVOT site by inhibiting sympathetic nerve activity.Objective: 1.To investigate the effect of PADN on canine cardiac autonomic activity and ventricular electrophysiological characteristics;2.To investigate the effect of PADN on LSG stimulation-induced ventricular arrhythmia(ventricular ventricular tachycardia).Methods: Twenty-one healthy adult male beagle dogs weighing 7-10 kg were randomly divided into experiment 1(n=11)and experiment 2(n=10).1.Protocol 1: to observe and analyze the effect of PADN on canine cardiac autonomic activity and ventricular electrophysiological properties.The changes of heart rate variability(including LF,HF,LF/HF),blood pressure(BP)and Effective refractory period(ERP)at the sites of ventricular apex,bottom and RVOT in 11 dogs were detected before and after PADN,as well as the LSG function,plasma levels of norepinephrine(NE),and angiotensin II(Angiotensin-II,Ang-II).2.Protocol 2: to observe and analyze the effect of PADN on ventricular arrhythmia induced by LSG stimulation in dogs and its possible mechanism.After successful establishment of a complete atrioventricular block model in 8 dogs,LSG was stimulated to record the occurrence of ventricular arrhythmia events before and after PADN,respectively.The other 2 dogs only underwent gross anatomy of the sympathetic anatomical connections between LSG and the pulmonary arteries.After euthanasia,the specimens of pulmonary arteries were treated with eosin staining(HE staining),tyrosine carboxylase(TH)staining,and choline acetyltransferase(ChAT)staining.Results: 1.Compared with the basal state,PADN can significantly increase HF,reduce the levels of LF,LF/HF and plasma levels of NE and Ang-II.What's more,PADN can prolong the ERP at the sties of left and right ventricles and RVOT(P<0.05),and significantly weaken ERP shortening induced by LSG stimulation at the RVOT site.The effect of PADN on LSG function is not clear,only the increase of systolic blood pressure caused by LSG stimulation(?20 V)can be reduced(P<0.05),and the steeply rising voltage-blood pressure response curve is significantly flattened,but the effect on diastolic pressure is next to nothing.2.LSG stimulation can significantly induce the occurrence of ventricular arrhythmia,and PADN can significantly weaken this effect of LSG stimulation.The number of premature ventricular contraction(PVC),ventricular tachycardia(VT)and the longest duration of a single sustained ventricular tachycardia were significantly reduced by PADN.3.Gross anatomy showed the presence of visible neurological connections between LSG and PA through the Ventromedial cardiac nerve(VMCN).Immunohistochemical staining of transverse sections of pulmonary arteries showed sympathetic nerve fibers enriched in the ventral wall of the pulmonary artery.Conclusion: PADN can attenuate cardiac sympathetic nerve activity,prolong ventricular ERP,and reduce the occurrence of ventricular arrhythmias caused by LSG stimulation,which is more selectively appeared at the site of RVOT.