摘要
背景:以往的血管损伤再狭窄模型大多在健康动物的正常血管上进行,研究仅仅针对正常动脉损伤后的愈合反应,而非粥样硬化血管壁球囊损伤后的反应,因此不能精确模拟人体血管成形术后的病理过程,不能完全反映人类疾病过程。目的:建立动脉粥样硬化大鼠颈总动脉球囊损伤模型,了解血管损伤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,观察术后不同时期血管内膜、中膜增生的改变并在透射电镜下观察血管壁超微结构。结果与结论:损伤后7 d新生内膜开始形成,至3个月时内膜增厚达最大,管腔明显狭窄,损伤动脉壁可见平滑肌细胞大量增殖。电镜下可见平滑肌细胞向"合成表型"转变,后期大部分恢复正常"收缩表型"。提示,应用球囊导管可以成功建立动脉粥样硬化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。
BACKGROUND： Animal models of vascular restenosis used to be established in the normal vessels, and study on the healing results limits in the normal artery, not atherosclerosis; thereby, the model cannot accurately simulate the pathological process after percutaneous transluminal coronary angioplasty. 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. The dynamic changes of neointimal and media hyperplasia were observed at different time points after surgery. Meanwhile, the ultrastructure of arterial wall was observed using transmission electron microscope. RESULTS AND CONCLUSION： The neointima formed at 7 days, and reached a peak at 3 months, vascular lumen was seriously narrow, and abundant smooth muscle proliferation could be found in the damaged artery wall. The smooth muscle cells switched from contractile type to synthetic type at the beginning after injury, and most of cells returned to contractile type finally. These findings indicate that 2.0 balloon catheter can successfully establish the carotid injury model in atherosclerosis rats; neointima hyperplasia results in lumen stenosis after injury; furthermore, phenotype transformation, proliferation, and migration of smooth muscle cells play an important role in the process of neointima hyperplasia.
出处
《中国组织工程研究》
CAS
北大核心
2016年第49期7334-7340,共7页
Chinese Journal of Tissue Engineering Research
