| Objective To investigate the effects of dexmedetomidine on atrial electrophysiological characteristics and Cx43 and Cx40 expression in rabbits after rapid atrial pacing. Methods Twenty-four adult male rabbits were selected and randomly divided into three groups:control group (Group C), rapid atrial pacing group (group RAP), and rapid atrial pacing + dexmedetomidine perfusion group (group RAP+DEX), with 8 rabbits in each group. Langendorff in vitro perfusion model was prepared, and atrial fibrillation model was established by rapid atrial pacing. The atrial monophasic action potentials after 90% calendar (MAPD90), the effective refractory period (ERP), the ratio of ERP to MAPD90 (ERP/MAPD90), and the induction rate and duration of atrial fibrillation in three groups were measured respectively. Finally, the protein content and distribution of Cx43 and Cx40 were detected by Western bolt and immunofluorescence method in the atrium tissues. Results At T1~T3, MAPD90 was compared among the three groups, and the difference was statistically significant (P<0.05). MAPD90 in group RAP showed a gradual downward trend over time, and different treatment methods and time had interaction effects on MAPD90 (P<0.05). At T3, the content of ERP, ERP/MAPD90, Cx43 and Cx40 in group RAP was lower than that in group C and group RAP+DEX, and the incidence of atrial fibrillation was higher than that in group C and group RAP+DEX (P<0.05). There was no significant difference in duration of atrial fibrillation among three groups (P>0.05). Under electron microscope, the distribution of Cx43 and Cx40 in group RAP was irregular and increased from the side, while the distribution of Cx43 and Cx40 in group C and group RAP+DEX was regular and mainly concentrated at both ends. Conclusion Dexmedetomidine can inhibit the atrial electrical remodeling in atrial fibrillation and reduce the susceptibility to atrial fibrillation. The mechanism may be related to the down-regulation and redistribution of Cx43 and Cx40. |
