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升主动脉缩窄大鼠左室心肌细胞结蛋白重构
Reconstruction of Desmin During Chronic Pressure Overload Cardiac Hypertrophy and Failure in Rats
【摘要】 目的 :通过观察左室心肌细胞结蛋白在升主动脉缩窄后心肌肥厚期和心力衰竭期的表达 ,探讨心肌肥厚和心力衰竭发生的机理。方法 :制作大鼠升主动脉缩窄动物模型 ,间接免疫荧光技术检测游离心肌细胞内结蛋白的分布 ,WesternBlot技术检测新鲜心肌组织中结蛋白的表达。结果 :心肌肥厚组和心力衰竭组左室心肌结蛋白表达与对照组相比明显增多 ;心力衰竭组结蛋白纤维在心肌细胞内的分布与对照组相比无明显差异。结论 :心肌细胞结蛋白表达的改变是慢性后负荷性心肌肥厚向心力衰竭转变的重要因素.
【Abstract】 Objective: Our aim was to observe the reconstruction of desmin during chronic overload cardiac hypertrophy and failure in rats with ascending aortic stenosis. Methods: Animal models of ascending aortic stenosis were made in female Wistar rats .The cardiac myocytes were isolated from left ventrium(LV). The immunofluorescent labeling of isolated myocytes and Western blotting analysis were used. Results: The expression of desmin protein in LV myocytes increased significantly in the group of cardiac hypertrophy and heart failure compared with controls (P<0.01). The distribution of desmin filaments didn’t change obviously compared with controls. Conclusion: The reconstruction of desmin in LV myocytes plays an important role in the transform of mechanical overload of cardiac hypertrophy to subsequent heart failure.
- 【文献出处】 中国医科大学学报 ,Journal of China Medical University , 编辑部邮箱 ,2003年03期
- 【分类号】R541
- 【被引频次】3
- 【下载频次】95