Model establishment and pathogenetic study of arterial restenosis in rats

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Model establishment and pathogenetic study of arterial restenosis in rats

更新时间：2024-01-17

- Model establishment and pathogenetic study of arterial restenosis in rats
- Journal of Chongqing Medical University Issue 4, Pages: 396-399(2002)
- 作者机构：
  
  重庆医科大学临床学院血管外科,重庆,400016
- 作者简介：
- 基金信息：
- DOI：
  CLC： R654.3
- Published：2002，
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[1]蒲庆华,时德,赵渝.大鼠颈动脉再狭窄模型的建立及其病理机制的初步研究[J].重庆医科大学学报,2002(04):396-399.

Model establishment and pathogenetic study of arterial restenosis in rats. [J]. Journal of Chongqing Medical University (4):396-399(2002)
[1]蒲庆华,时德,赵渝.大鼠颈动脉再狭窄模型的建立及其病理机制的初步研究[J].重庆医科大学学报,2002(04):396-399. DOI：

Model establishment and pathogenetic study of arterial restenosis in rats. [J]. Journal of Chongqing Medical University (4):396-399(2002) DOI：

摘要

目的：建立再狭窄动物模型，研究再狭窄的发生规律及病理机制。方法：模拟临床PTCA过程，造成大鼠颈动脉扩张损伤，在此基础上系统地观测术后不同时相点内膜、中膜的增生以及细胞增殖的动态变化规律，并应用透射电镜对术后不同时期血管壁的超微结构、平滑肌细胞（VSMC）的功能状态进行了动态观测。结果：损伤后动脉壁新生内膜于术后14～28天增厚达高峰；损伤动脉壁细胞大量增殖，中膜、内膜增殖指数分别于术后4天、9天达到峰值；增生动脉壁内膜及中膜的大部分细胞α-actin染色阳性，而CD68染色阴性；损伤早期平滑肌细胞胞浆中肌丝成分明显减少，细胞器明显增多。结论：损伤动脉因新内膜过度增生导致管腔狭窄。VSMC的转型、增殖、迁移和分泌胞外基质是动脉过度增生的病理基础。

Abstract

Objective: To establish an arterial restenotic model

and to study the pathogenesis of restenosis after angioplasty. Methods: The balloon catheter injury was performed on left common carotidartery of rat by imitating the process of angioplasty. The process of neointimal and media hyperplasia was observed and the proliferation index of vascular smooth muscle cell (VSMC) at different time after operation was measured. The change of phenotype of VSMC in injured arteries was also surveyed with electron microscope. Results: Arterial neointima hyperplasia occurred after injury and reached to summit at 14 to 28 d. Cell proliferation attained a maximum at 4 day in the media (43.92%) and at 9day in the intima (63.98%). Immunostain of CD68 was negative whereas α-actin was mostly positive in the neointimal and medial cells. Ultrastructurally

the bulk of cytoplasm of VSMCs was filled with organelles with scattered myofilaments peripherally located. Conclusion:Neointima hyperplasia occurs after balloon injury and results in lumen stenosis. VSMC phenotype transformation

proliferation

migration

and extracellular matrix production are the key celllaur processes in this lesion.

关键词

再狭窄动脉成形术血管平滑肌大鼠

Keywords

restenosisAngioplastyVascular smooth muscle cellrat

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