The Effect And Underlying Mechanism Of Selective Cardiac Sympathetic Afferent Denervation On Ventricular Arrhythmias In The Canine Model Of Acute Myocardial Ischemia

OBJECTIVES To investigate whether cardiac sympathetic afferent denervation(CSAD)could protect against ventricular arrhythmias(VAs)by modulating cardiac sympathetic nerve activity in an acute myocardial ischemia(AMI)canine model.METHODS Thirty anesthetized dogs were assigned to the sham group(n=8),the AMI group(n=13)and the CSAD group(n=9)randomly.CSAD was produced by epicardial application of resiniferatoxin and the vehicle was applied to the epicardium as a control.Heart rate variability(HRV),plasma norepinephrine(NE)concentration,left stellate ganglion(LSG)neural activity,effective refractory period(ERP)of ventricles,ERP dispersion,ventricular action potential duration(APD),APD dispersion,beat-to-beat variability of repolarization(BVR)were determined at baseline and after intervention.We produced an AMI model by occluding the left anterior coronary artery,and performed analysis of VAs for 60 min using electrocardiography.The above indicators will be repeated including the detection of APDA cycle length and LSG function after AMI.Then,levels of c-fos and nerve growth factor(NGF)were determined.RESULTS There was no significant difference at the baseline among three groups.Compared with sham group,CSAD significantly increased HRV,decreased serum NE level,attenuated LSG activity,prolonged ventricular ERP and APD,and decreased BVR of APD in the CSAD group,whereas no significant change was shown in the AMI group.AMI resulted in a significant decrease in HRV,increase in serum NE level,LSG function,LSG activity,reduction in ERP and APD of ischemic ventricle,elevation in ERP dispersion,APD dispersion and BVR,and increase in the APDA cycle length in the AMI group,which were attenuated in the CSAD group.The incidence of VAs was significantly lower in the CSAD group than in the AMI group.Compared with the AMI group,the expression of c-fos and NGF protein in the LSG after AMI was significantly lower in the CSAD group.CONCLUSION CSAD can suppress cardiac sympathetic neural activity,thereby increasing electrophysiological stability and protecting against AMI-induced VAs.