动脉粥样硬化大鼠血管损伤后局部组织学结构的变化

目的建立大鼠颈总动脉球囊损伤模型，了解血管成形术后再狭窄的发生规律及病理机制。方法在大鼠动脉粥样硬化病变的基础上，使用2F球囊导管损伤大鼠左侧颈总动脉，观察术后不同时期内膜、中膜增生的动态改变；对血管壁增殖的细胞进行鉴定；观察血管壁平滑肌细胞表型标志物SMα—actin表达的变化。结果损伤后7天薪生内膜开始形成，至3月时内膜增厚达最大，管腔明显狭窄，损伤动脉壁可见细胞大量增殖，大部分为平滑肌细胞。损伤早期血管壁表达SMα—actin减少，至损伤后期逐渐恢复至原有水平。结论应用球囊导管可以成功建立大鼠血管损伤动物模型，损伤后新生内膜增生导致管腔狭窄，平滑肌细胞的表型改变、迁移及增殖是内膜过度增生的病理基础。

The Changes of Histochemistry of Arterial Wall in Atherosclerosis Rats After Carotid Injury

Objective To establish the common carotid catheter injury model in atherosclerosis rats and to study the pathogenesis of restenosis. Methods The balloon catheter injury was performed on the left common carotid artery of atherosclerosis rats with 2F balloon catheter. HE and Verhoeff staining were used to observe the dynamic change of neointimal and media hyperplasia at different time after injury. Immunohistochemistry was used to detect the proliferative cells and the change of SMα - actin expression. Results （1） At 7 days, the neointima formed and continuously thickened. At 3 months, the neointimal thickening reached a peak and vascular lumen was seriously narrow. Immunostain of SMα - actin was mostly positive in the neointimal and medial cells which show most of proliferative cells are smooth muscle ceils. （2） The expression of SMα - actin was decreased from 2 days after balloon injury and then increased at 3 months. Conclusion Using of 2.0 balloon catheter can successfully establish the rat carotid injury model. Neointima hyperplasia occurs after balloon injury and results in lumen stenosis. VSMC phenotype transformation, proliferation, migration and extracellular matrix production play an important role in the processe of neointima hyperplasia.