2009•Unpublished venueRequires access
Study of the atrial fibrosis and the expression of PDGF receptor-β during atrial fibrillation
Yuansheng Liu
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Abstract
【Objective】To investigate the possible mechanisms of atrial fibrosis during atrial fibrillation.Meth-odsFifteen adult mongrel dogs were randomly divided into 3 groups:control group, pure atrial fibrillation group and atrial fibrillation + mibefradil group.Van-Gieson staining, immunohistochemical method combined with High-resolution color image analysis system were used to detect the expressions total cardiac collagen, cardiac collagen subtype Ⅲ and PDGF receptor-β subunit in the three groups.【Results】The total cardiac collagen was significantly higher in pure atrial fibrillation group and atrial fibrillation + mibefradil group when compared with that of control group(P 0.05).The expression of total cardiac collagen in atrial fibrillation + mibefradil group was significantly lower than that of pure atrial fibrillation group(P 0.05).The expression of cardiac collagen subtype Ⅲ was significantly higher in pure atrial fibrillation group than that of control group(P 0.05).The expression of cardiac collagen subtype Ⅲ in atrial fibrillation + mibefradil group was significantly lower than that of pure atrial fibrillation group(P 0.05).The expression of PDGF receptor-β subunit in atrial fibrillation group was decreased than that of control group(P 0.05).The expression of receptor-β subunit in atrial fibrillation + mibefradil group was greatly decreased than that of atrial fibrillation group(P 0.05).ConclusionAtrial fibrosis was observed in atrial tissues during persistent atrial fibrillation, which could be relieved by T-type Ca2+ channel blocker.The expression of PDGF receptor-β subunit was decreased with persistent atrial fibrillation lasting for 6 months.