持续性心房颤动心肌纤维化实验探究.docVIP

持续性心房颤动心肌纤维化实验探究 　 作者：崔明玉， 郭琳娜， 姜丽萍， 陈阿梅 【摘要】 目的 探讨心房颤动心肌纤维化的发生机制。方法 杂种犬15条，随机分三组：正常对照组、单纯房颤组、房颤+Miberfradil组。采用van Gieson染色、免疫组织化学方法，结合高清晰彩色图像分析系统，观察正常对照组、单纯房颤组和房颤+Miberfradil组心房组织总胶原、Ⅲ型胶原的表达。结果 （1）单纯房颤组和房颤+Miberfradil组心房组织总胶原均明显高于正常对照组（P＜0.05）。房颤+Miberfradil组的总胶原表达明显减少，与单纯房颤组相比较，差异有显著性（P＜0.05）。（2）单纯房颤组Ⅲ型胶原的表达明显高于正常对照组（P＜0.05）。房颤+Miberfradil组Ⅲ型胶原的表达明显低于单纯房颤组（P＜0.05）。结论 持续性房颤有明显的心肌纤维化改变，T型钙通道阻滞剂能够减轻心肌纤维化的程度。 【关键词】 心房颤动；心肌纤维化；胶原纤维 【Abstract】 Objective To investigate the mechanisms of the cardiac fibrosis during atrial fibrillation. Methods Fifteen adult mongrel dogs were randomly divided into 3 group: pure atrial fibrillation group, atrial fibrillation added mibefradil group and control group. van-Gieson stain was used to detect total cardiac collagen. Cardiac collagen subtype Ⅲ were studied by immunohistochemistry and image analysis. Results （1）Total cardiac collagen was significantly increased in pure atrial fibrillation group and atrial fibrillation added mibefradil group compared with that of control group （P＜0.05） . Total cardiac collagen markedly decreased in atrial fibrillation added mibefradil group compared with that of pure atrial fibrillation group（P＜0.05）.（2） 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 was markedly lower in atrial fibrillation added mibefradil group than that of pure atrial fibrillation group （P＜0.05）. Conclusion Cardiac fibrosis was observed during persistent atrial fibrillation and it was relieved by T-type calcium channel blocker. 【Key words】 atrial fibrillation; cardiac fibrosis; collagen fiber 心房颤动是临床常见的心律失常，并发症严重。持续性房颤可以引起心房的结构重构，表现为心肌纤维化、心肌细胞肥大，部分肌溶解现象［1］。这些改变成为房颤发生过程中兴奋传导障碍和加重功能障碍的结构基础。到目前为止，对于房颤心肌纤维化的发生机制尚不清楚。本文采用van Gieson染色、免疫组织化学方法，结合高清晰彩色图像分析系统，研究持续性房颤心房组织胶原表达的变化，探讨房颤心肌纤维化的机制，为临床治疗和防止房颤的复发提供理论依据。 1 材料与方法 1.1 动物模型 杂种犬15条，体重22～28kg，雌雄不拘，由中国人民解放军总医院提供。随机分三组，每组5条。分为正常对照组、单纯房颤组、房颤+Mibe