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目的探讨动脉损伤后内膜平滑肌细胞增殖状态下的凋亡细胞的水平及其出现的时间的部位，深入地研究血管成形术后再狭窄的形成机制，为抑制再狭窄的形成提供可能的干预措施。方法和结果应用球囊导管损伤小型猪髂动脉制备成内膜增殖所致的血管狭窄模型，采用计算机彩色图像分析系统动态观察损伤后１天、３天、６天、１２天和３０天的内膜平滑肌细胞增殖状况，并用末端转移酶介导的ｄＵＴＰ标记在ＤＮＡ３′－ＯＨ的方法（ＴＵＮＥＬ）来标记凋亡细胞。结果表明，损伤后６天以内，未出现凋亡细胞，从１２天起，仅在增殖的内膜中出现了较低水平的凋亡，即１２天（１．９４±０．４２）％和３０天（１．３６±０．３１）％，后二者差异无显著性。可以认为，较低水平的凋亡细胞可能是再狭窄形成过程中的病理学特征。结论平滑肌细胞的凋亡是血管损伤后狭窄形成过程中的一个重要的病理学特征，相比大量增殖的内膜平滑肌细胞，较低水平的凋亡可能是血管狭窄形成的机制之一，这提示，对低水平的凋亡进行适时适量的诱导，可能为抑制再狭窄提供新的选择。
OBJECTIVE: To investigate the level of apoptosis cells in proliferating state of intimal smooth muscle cells after arterial injury and the location of their appearance in time. To study the formation mechanism of restenosis after angioplasty and to provide possible interventions for inhibiting the formation of restenosis . Methods and Results The model of vascular stenosis induced by intimal hyperplasia was established by balloon catheter injury to the iliac artery. The colorimetric analysis system was used to observe the changes of the vascular lesion within 1 day, 3 days, 6 days, 12 days and 30 days after injury Membrane smooth muscle cell proliferation and labeling of apoptotic cells with the method of telomerase-mediated dUTP labeling in DNA3’-OH (TUNEL). The results showed that within 6 days after injury, apoptotic cells did not appear, and from the 12th day, only a small amount of apoptosis appeared in proliferating endometrium, that is, 12 days (1.94 ± 0.42)% and 30 days (1.36 ± 0.31)%, the difference between the latter two was not significant. It is believed that lower levels of apoptotic cells may be pathological features of restenosis. Conclusions Apoptosis of smooth muscle cells is an important pathological feature of stenosis after vascular injury. Lower apoptosis may be one of the mechanisms of vascular stenosis than that of proliferating endometrial smooth muscle cells , Moderate and timely induction of low level of apoptosis may provide a new option for inhibiting restenosis.