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经皮腔内血管成形术后再狭窄与血管内皮细胞的关系

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经皮腔内血管成形术(PTA)是治疗冠状动脉及周围动脉狭窄的有效手段,但约有25%~60%的病人术后发生再狭窄。金属内支架的应用降低了PTA术后急性闭塞的发生率,但并未能彻底解决再狭窄的问题。大量实验研究及临床观察表明再狭窄与血栓形成、内膜增厚和血管重构有关,内皮细胞的损伤、修复及功能改变在其中扮演重要角色。

关键词: 血管,成形术,再狭窄,内皮细胞

一、内皮损伤、血栓形成与再狭窄
PTA可造成血管损伤,内皮的剥脱造成内皮下组织的暴露,血小板立即通过Von Willebrand因子(VWF)黏附于内皮下的基质,随后发生聚集并释放α颗粒成分,其释放的血小板衍生生长因子(PDGF)可能与中膜平滑肌细胞的激活和迁移有关[1]。最近的研究表明血小板减少可抑制已激活的平滑肌细胞从中膜向内膜迁移。由内皮损伤引发的凝血过程将形成附壁血栓,血栓的形成不仅可造成血管的急性闭塞,而且为平滑肌细胞内迁提供了框架,血栓的机化可直接引起内膜增厚,而且血栓中的凝血酶本身就是强力的平滑肌细胞致分裂原[2]。实验证明损伤部位内皮的早期重建可抑制血小板附着和血栓形成[3]。
目录:
  一、内皮损伤、血栓形成与再狭窄

  二、内皮细胞和内膜增厚

  三、内皮细胞与血管重构

  四、内皮细胞损伤、修复及功能异常

  五、加快重内皮化、促进内皮细胞功能恢复

六、金属内支架和血管内皮化


参考文献:
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