摘要
目的 :探讨血管球囊损伤后内膜增殖的机制。方法 :采用电镜、末端脱氧核苷酸转移酶介导的三磷酸脱氧尿嘧啶缺口末端标记法 (TUNEL)和免疫组织化学技术检测球囊损伤后血管平滑肌细胞 (VSMC)凋亡及新生内膜面积的变化。结果 :球囊损伤后血管壁增生 ,球囊损伤后第 3天 ,血管中层出现凋亡的平滑肌细胞 (SMC) ;损伤后第 7天 ,新生内膜形成 ,内膜和中层SMC凋亡率最高 ,凋亡的SMC主要分布在内膜层 ,以后逐渐降低 ;至损伤后第 2 8天 ,仅内膜层有少量凋亡的SMC ;血管紧张素Ⅱ 1型受体 (AT1R )拮抗剂Irbesartan显著增加SMC凋亡和抑制内膜增生。结论 :VSMC凋亡不足是球囊损伤后血管内膜增生的机制之一。
Objective: To investigate the mechanism of intima hyperplasia after balloon injury of a vessel Methods: The percentage of apoptosis of vascular smooth muscle cells (VSMCs) and the area of neointima were determined with electron microscopy, TUNEL and immunohistochemical assay Results: After balloon injury, the vascular wall was thickened On the 3rd day after injury, apoptosis of VSMCs appeared in the vascular media and neointima was formed on the 7th day On that day, apoptosis of VSMCs in the vascular intima and media reached the peak The apoptotic VSMCs distributed mainly in the intima Then the number of apoptotic VSMCs gradually decreased and there were a few apoptotic cells in the intima on the 28th day after balloon injury Irbesartan, an antagonist of angiotension Ⅱsubtype Ⅰ, significantly increased apoptosis of VSMCs and suppressed the proliferation of intima Conclusion: Insufficient apoptosis of VSMCs is the important mechanism of intima hyperplasia after balloon injury of the vessels
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2000年第3期268-271,共4页
Journal of Third Military Medical University
