| Objective To evaluate the expression of atrial muscle gap junction Cx40in rheumaticheart disease with chronic atrial fibrillation by using the new class III antiarrhythmicdrug ibutilide specific block ultra-rapid delayed rectifier potassium channels(Kv1.5),todiscuss possibility of the Kvl.5potassium channels to be one of downstream signaltransduction pathways of the atrial muscle gap junction protein,and to reveal thepossible mechanism of atrial fibrillation(AF).Methods The experiment specimens were taken from right atrial appendage tissue of rheumatic heart disease who accept the valve replacement surgeries,and these specimens were divide into2groups according to the heart rate before surgeries:The sinus rhythm group of rheumatic heart disease Sinus rhythm (SR) group,and the atrial fibrillation group of rheumatic heart disease heart disease(AF group).Enzyme was used to dissociate atrial myocytes,atrial myocytes was cultured and Western blot was used to detect the protein expressions of Cx40in two groups before and after they were selective acted on by the selective Kvl.5potassiumchannel blocker-ibutilide.Results After using the Class III antiarrhythmic agents to selective act on Kvl.5potassium channel in rheumatic heart disease with chronic atrial fibrillation,the expression of Cx40was significantly higher in AF group (P<0.01).The protein expression of Kv1.5was not significantly changed in SR group. Conclusion In the group of rheumatic heart disease with atrial fibrillation,the ex-pression of Cx40was significantly increased after using the a specific inhibitorof Kv1.5potassium channel blocker in AF group,proving that the open Kv1.5po-tassium channels may affect the expression of connexin Cx40,which further reveals that electrical remodeling may lead to the diversification of structural remodel-ing in AF. |
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