A study of blocking intermediate-conductance calcium-activated potassium channel in cardiac ganglionated plexi decreased atrial fibrillation vulnerability in canines with rapid atrial pacing
A study of blocking intermediate-conductance calcium-activated potassium channel in cardiac ganglionated plexi decreased atrial fibrillation vulnerability in canines with rapid atrial pacing
Objective To explore the role of conductance calcium activated potassium channel(KCa3.1)in the pathogenesis of atrial fibrillation(AF)by mediating macrophage polarization in cardiac ganglionated plexi(GP).Methods The study was conducted at the Cardiovascular Research Institute of Wuhan University in 2023.Eighteen beagles were randomly divided into the control group(n=6),rapid atrial pacing(RAP)group(n=6)and TRAM-34(a KCa3.1 blocker)group(n=6)according to the random number table method.TRAM-34(0.3 ml,15 mmol/L)and saline were locally injected into GPs in the TRAM-34 group dogs and the other groups,respectively.After that,the neural activity of anterior right GP(ARGP)and atrial electrophysiology were measured.The levels of inflammatory factors and the function of macrophages in ARGP were detected in the three groups then.Results There were no significant effects on atrial electrophysiology and ARGP activity in the non-pacing dogs after injection of TRAM-34.The RAP shortened effective refractory period(ERP)values at all sites and increased the AF vulnerability and ARGP neural activity,while TRAM-34 treatment reversed these changes.The levels of CD68+cells,induced nitric oxide synthase(iNOS),interleukin(IL)-1β,IL-6 and tumor necrosis factor(TNF)-α in ARGP were higher in the RAP group and the TRAM-34 group than those in the control group.Furthermore,the levels of the CD68+cells,iNOS and inflammatory cytokines in ARGP were higher in the RAP group than those in the TRAM-34 group.Conclusions During RAP,blocking KCa3.1 could inhibit the GP activity and reduce the AF vulnerability,which might be related to the reduced inflammatory response in GP mediated by local macrophages.
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