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目的:探讨肥胖对家兔心房肌组织结构和电生理特性的影响,为进一步了解肥胖影响房颤(AF)易感性的相关机制和AF的早期干预提供实验依据。方法:将30只家兔随机分为正常组、肥胖组和肥胖+他汀药物组,雌雄各半,每组10只。肥胖组给予高脂饲料,造模成功后,采用Langendorff离体灌注法对3组家兔分别进行离体心脏灌注。采用心脏电生理刺激仪监测心房肌的电生理特性参数:肥胖组家兔房内传导时间(HRA-HIS)、心房有效不应期(AERP)、窦房结恢复时间(SNRT)、校正后窦房结恢复时间(CSNRT)。剪取部分心耳组织,经MASSON染色观察心房肌纤维化的程度。采用TUNEL法测定心房肌细胞的凋亡率。结果:与正常组相比,肥胖组家兔HRAHIS、AERP、SNRT和CSNRT等电生理参数均出现不同程度的延长,并导致AERP频率自适应性降低。与肥胖组比较,肥胖+他汀药物组的心肌基质胶原纤维显著减少(P<0.05),心肌胶原容积分数(CVF)显著减低(P<0.01),心肌细胞凋亡率(%)明显降低(P<0.01)。结论:肥胖可引起家兔心房肌组织结构与电生理基质改变,利于AF的发生与维持,而应用他汀类药物干预后,这些改变有所改善。
OBJECTIVE: To investigate the effect of obesity on the structure and electrophysiological characteristics of atrial myocardium in rabbits, and to provide experimental evidence for further understanding the mechanism of obesity on the susceptibility of atrial fibrillation (AF) and the early intervention of AF. Methods: Thirty rabbits were randomly divided into normal group, obesity group and obesity + statin group, with 10 male and one female, respectively. Obese rats were given high-fat diet. After successful model establishment, Langendorff perfusion was used to perfuse isolated heart from each group. Electrophysiological parameters of atrial myocardium were monitored by electrophysiology stimulator: HRA-HIS, AERP, SNRT, corrected sinus Room Recovery Time (CSNRT). A part of the atrial appendage was cut out and the extent of atrial fibrosis was observed by MASSON staining. Apoptosis rate of atrial myocytes was measured by TUNEL method. Results: Compared with the normal group, the electrophysiological parameters such as HRAHIS, AERP, SNRT and CSNRT in obese group all increased to different extents, and resulted in the decrease of AERP frequency adaptively. Compared with the obese group, the myocardial matrix collagen fibers in the obese + statin group were significantly decreased (P <0.05), the myocardial collagen volume fraction (CVF) was significantly decreased (P <0.01) and the myocardial apoptosis rate <0.01). CONCLUSION: Obese can cause changes of atrial muscle tissue and electrophysiological matrix in rabbits, which contributes to the occurrence and maintenance of AF. However, these changes are improved after intervention with statins.