论文部分内容阅读
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 intimal hyperplasia after vascular balloon injury. Methods: The apoptosis and neointimal area of balloon injured vascular smooth muscle cells (VSMCs) were detected by electron microscopy, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) and immunohistochemistry The change. Results: Apoptotic smooth muscle cells (SMCs) were found in the middle vascular layer on day 3 after balloon injury. The apoptosis rate of neointimal formation, intima and middle SMC was highest on the 7th day after injury , The apoptotic SMC mainly distributed in the endometrium and then gradually decreased; only a small amount of apoptotic SMCs were found in the intima on day 28 after injury; Irbesartan, an angiotensin Ⅱ type 1 receptor (AT1R) antagonist, was significantly Increase SMC apoptosis and inhibit intimal hyperplasia. Conclusion: Insufficient VSMC apoptosis is one of the mechanisms of intimal hyperplasia after balloon injury.