Expression Of CalpainⅠ In Pulmonary Vein Myocardial Sleeves And Left Atrium In A Canine Model Of Persistent Atrial Fibrillation By Rapid Pulmonary Vein Pacing

Atrial fibrillation(AF) is the most common cardiac arrhymia,it severely damaged the health of the affected patients by causing stroke, decreasing heart function and developing myocardial disease.Nowadays, the pathogenesis of AF has been the hot spot of the research in the cardiovascular domain.It has been generally recognized that the electrical and histological remodeling in the pulmonary vein myocardial sleeves and left atrium (LA)has played a basilic role in the maintenance and stabilization of the persistent AF. CalpainⅠis the representative protein kinase in the Calpain family.Studies have indicated that the change of CalpainⅠin the left atrium has played a key role in the maintenance and stabilization of the AF. However, there were seldom studies about the expression of the CalpainⅠin the pulmonary vein myocardial sleeves. In this study,we establish a persistent AF model of canine by rapid pulmonary vein pacing and identify the changes of CalpainⅠmRNA and protein level in pulmonary veins and left atrium, so that it was intended to investigate the role of CalpainⅠon the maintenance and stabilization of AF and provided useful clues for the clinic therapy of persistent AF. Objective:1,To establish a persistent AF model of canine by rapid pulmonary vein pacing.2,To identify the expression of CalpainⅠin the pulmonary veins and left atrium in persistent AF in order to investigate the role of CalpainⅠon the maintenance and stabilization of AF. Method: 1,Fifteen mongrel dogs were instrumented with annular pacing electrodes on the left superior pulmonary vein(LSPV) and mapping electrodes patches on the left atrium .The annular pacing electrodes were connected in a home-made stimulator with chronic rapid pulmonary vein pacing. Programmed electrical stimulation and burst pacing technique was used to examine whether the time of AF last more than 24h. 2,The mRNA and protein expression of CalpainⅠin pulmonary veins and left atrium were assessed by reverse transcriptase PCR and Western blot respectively. Result: 1,Persistent AF(>24h) was induced in eleven of fifteen canines within 28.2±3.0 days. 2,No significant differences were found in the expression of CalpainⅠbetween the normal left upper pulmonary and left atrium. The mRNA and protein expressions of CalpainⅠincreased dramatically in the AF group than that in the SR group,either in pulmonary veins or left atrial.In the AF group, the mRNA and protein expressions of CalpainⅠincreased dramatically in pulmonary veins than that in left atrium. Conclution:There was remodeling of CalpainⅠin pulmonary veins and left atrial during AF,and the remodeling is involved in the maintenance and stabilization of AF.The therapy aims at the CalpainⅠmay provide useful clues for the clinic therapy of persistent AF.