Rekhter M D, Mironov A A, Anisimov V M
Arkh Anat Gistol Embriol. 1991 Feb;100(2):24-30.
An experimental model of repeated cryogenic lesions in the rat abdominal aorta endothelium with a concentrically decreasing area of the defect has been worked out. In reendothelization of every successive defect participate the cells of the endothelial layer that is formed anew after the preceding lesions. As a result of repeated lesions the regeneration rate increases by 1.2 times. By means of scanning radioautography after 3H-thymidine++ administration the index of the labelled nuclei of the endothelial cells (EC) has been demonstrated to increase by 2.2 times. In the experiments with gamma-irradiation of the vessel before the last cryodestruction (this results in blockade of proliferation) an increased rate of EC migration has been revealed. Repeated lesions also produce an increase in the heteromorphism degree of the endothelial layer. This is mainly manifested as appearance of multinuclear EC clusters. These changes in rate and in character of the endothelium regeneration can be determined by the mechanisms similar to clonal proliferative senescence of EC in vitro.
已建立一种大鼠腹主动脉内皮反复低温损伤的实验模型,损伤缺损面积呈同心递减。在前一次损伤后重新形成的内皮层细胞参与到每一个连续缺损的再内皮化过程中。反复损伤使再生率提高了1.2倍。给予³H - 胸腺嘧啶核苷后,通过扫描放射自显影法显示内皮细胞(EC)标记核指数增加了2.2倍。在最后一次冷冻破坏前对血管进行γ射线照射的实验中(这导致增殖受阻),发现EC迁移速率增加。反复损伤还会使内皮层的异质性程度增加。这主要表现为多核EC簇的出现。内皮再生速率和特征的这些变化可能由类似于体外EC克隆增殖衰老的机制所决定。