Olsen E G, Davanger M
Acta Ophthalmol (Copenh). 1984 Oct;62(5):796-807. doi: 10.1111/j.1755-3768.1984.tb05808.x.
A circular 4 mm endothelial defect was induced by transcorneal freezing. The experimental damage and the healing took place in the living rabbit in 15 eyes, and in the isolated cornea in organ culture in further 20 eyes. The reparative process was studied by SEM, and proved to be the same in vivo and in vitro. The defect was covered with endothelial cells after 3 days. The normal hexagonal pattern was regained after 3 weeks. Both cell migration and cell division were involved in the reparative process. Only cells recruited from a zone close to the defect were active; the cells situated more than a few cell diameters from the original edge maintained their form and size unchanged. The first phase of cell division was the formation of a spherical cell with numerous blebs on its surface.
通过经角膜冷冻诱导出一个直径4毫米的圆形内皮缺损。在15只活兔眼中进行了实验性损伤及愈合过程的观察,另外20只眼在器官培养的离体角膜中进行观察。通过扫描电子显微镜研究修复过程,结果证明在体内和体外的修复过程是相同的。缺损在3天后被内皮细胞覆盖。3周后恢复了正常的六边形形态。细胞迁移和细胞分裂都参与了修复过程。只有从缺损附近区域募集的细胞才活跃;距离原始边缘超过几个细胞直径的细胞保持其形态和大小不变。细胞分裂的第一阶段是形成一个表面有许多小泡的球形细胞。