摘要
目的通过观察大鼠心肌梗死后心肌细胞增殖分化、心肌肌动蛋白表达水平改变情况,探讨其在梗死后心肌重塑中的地位与可能的生物学意义。方法结扎大鼠左冠状动脉制备心肌梗死模型,观察大鼠心肌梗死后血流动力学及心肌组织病理形态改变评估梗死面积;荧光免疫法检测核分裂指数及心肌肌动蛋白表达量。结果大鼠心肌梗死后左心室舒张、收缩功能均下降;与对照组相比,心肌细胞核分裂指数增加了1.24、2.00、2.23、2.20和1.89倍(均为P<0.01);保留有丝分裂能力心肌细胞主要存在于维持着较充足的血氧供应的缺血边缘及缺血远端心肌;非梗死区域肌动蛋白表达水平在心肌梗死后7、14和30d分别增加了1.12、1.25和1.23倍(均为P<0.05)。结论心肌梗死所致的心肌细胞丧失激活了心肌细胞的分裂增殖,同时心肌肌动蛋白表达增加,二者共同参与了非梗死区域心肌肥厚与心室重塑的发生发展,维持病理状态下的心脏功能。
Objective To study the consequences of the proliferation and differentiation of myocytcs and myocardial actin expression after myocardial infarction in rats and the possible biological significance in myocardial remodeling. Methods Rats＇ myocardial infarction （MI） models were mimicked by ligation of the left coronary artery. Hemodynamics and the pathological changes of myocardial tissue were observed to assess the infarct size. Immunofluorescence microscopy was used to examine the change of the myocyte mitotic index and the expression of actin. Results The left cardiac dystolic and systolic function declined after MI. Compared with the control group,the myocyte mitotic index was 1.24-fold ,2.00-fold ,2.23-fold ,2.20-fold and 1.89-fold （ P 〈 0.01 for each ）. The myocyte of mitosis existed in the ischemic edge with sufficient blood and oxygen supply and the distal myocardial myocyte. The myocardial actin expression in the non-infarction area was 1.12-fold, 1.25-fold and 1.23-fold higher at 7 days, 14 days and 30 days （ P 〈 0.05 for each）. Conclusion Loss of myocytes caused by MI activates the proliferation of myocardial myocytes and advocates the increased expression of actin, both of which are involved in the development of myocardial hypertrophy and myocardial remodeling in non infarct area, maintaining the cardiac function under pathological condition.
出处
《中国综合临床》
北大核心
2006年第6期481-484,共4页
Clinical Medicine of China
基金
国家重点基础研究发展计划(973计划
2003CB517104)
湖北省卫生厅医药卫生科研计划项目(鄂卫发[2003]103号/JX1B141)
