Mechanism Of Low-level Vagal Nerve Stimulation In Intervention Of Atrial Fibrillation Induced By Acute Obstructive Sleep Apnea In Dogs

Objective: To investigate the mechanism of low-level vagus nerve stimulation(LL-VNS)in the treatment of atrial fibrillation(AF)induced by obstructive sleep apnea(OSA)in dogs.Methods: 18 adult male healthy mongrel dogs were randomly divided into three groups: control group(n=6),OSA group(n=6)and OSA + LL-VNS group(n=6).All animals were intubated under general anesthesia.The OSA group and the OSA + LL-VNS group were simulated the OSA procedure artificially,which was suffocated for 2minutes,ventilated for 8minutes,and 10 minutes was a cycle lasting 6 hours.The OSA + LL-VNS group was given LL-VNS from the third hour to the end of the experiment and the control group was not suffocated.The changes of blood gas indexes at 0h,1h,3h,6h and inflammatory markers including TNF-α,IL-2 and IL-6 at 0h,3h and 6h after modeling were detected.The canine arterial blood pressure was recorded throughout the whole experiment.At the end of the experiment,the atrial muscle tissue was taken for hematoxylin-eosin staining(HE).Results: Successful establishment of an acute OSA canine model(P < 0.05).Compared with the control group,acute OSA resulted in shortening of atrial ERP,prolongation of AF duration,prolongation of SNRT,increase of left atrium,mitochondrial edema,increase of cardiomyocyte apoptosis,decrease of Cx43 expression,expression of TH and ChAT Enhanced,the above were statistically significant(P < 0.05).However,LL-VNS reversed the above changes to a certain extent,both of which were statistically significant(P < 0.05).However,LL-VNS had little effect on changes of systolic blood pressure induced by OSA.HE staining in OSA,OSA and OSA +LL-VNS groups showed no significant changes.Conclusions: LL-VNS effectively inhibited the electrical remodeling,structural remodeling,and nerve remodeling in the atria of acute OSA dogs by prolonging ERP in the atria,suppressing inflammatory responses of the body,and expressing TH and ChAT,and increasing the expression level of Cx43.