IInfluence of obesity on rabbit atrial muscle tissue structure and electrical physiological characteristics[J]. Chinese Heart Journal, 2014, 26(1): 24-28.
    Citation: IInfluence of obesity on rabbit atrial muscle tissue structure and electrical physiological characteristics[J]. Chinese Heart Journal, 2014, 26(1): 24-28.

    IInfluence of obesity on rabbit atrial muscle tissue structure and electrical physiological characteristics

    • AIM:To explore the influence of obesity on rabbit atrial muscle tissue structure and electrical physiological characteristics and to better understand the mechanism of atrial fibrillation (AF) susceptibility induced by obesity and to provide an experimental basis for early intervention AF. METHODS: Thirty rabbits were randomly divided into three groups: normal group, obesity group and obesity statin group, with ten rabbits in each group. After the successful establishment of the obesity model, Langendorff perfusion in vitro was used for rabbit heart perfusion in vitro. The cardiac electrophysiological stimulator was then used to detect the electrical physiological characteristic parameters including atrium room conduction time (HRA-HIS), atrial effective refractory period (AERP), sinoatrial node recovery time (SNRT), and corrected sinoatrial node recovery time (CSNRT). After shearing part of the rabbit auricle tissue, atrial muscle fibrosis was observed using Masson stain and atrial muscle cell apoptosis was detect by TUNEL. RESULTS: The electrical physiological parameters including HRA-HIS, AERP, SNRT and CSNRT were all extended to some degree and AERP frequency adaptability significantly reduced in obesity group. The myocardial matrix collagen fiber and CVF obviously decreased, whereas cardiomyocyte apoptosis rate significantly increased in the obesity group compared with those in the obesity statin group (all P<0.05). CONCLUSION: Obesity can change the rabbit atrial muscle tissue structure and electrical physiological characteristics, which is propitious to the occurrence and maintenance of AF.
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