Chan-Ling T, Tout S, Holländer H, Stone J
Department of Anatomy, University of Sydney, Australia.
Invest Ophthalmol Vis Sci. 1992 Jun;33(7):2128-47.
This study documents changes to retinal vasculature during the feline form of retinopathy of prematurity (ROP). The authors describe the closure and obliteration of retinal vessels during exposure to high oxygen, the pattern and tempo of growth of proliferative vasculature, which, after the return of the animal to room air, extends from the optic disc in a spectacular "rosette" pattern, the formation of preretinal vascular growths, and an initial lack of barrier properties in the new vessels. Finally, the response of the vasculature to the relief of hypoxia is reported, including the gradual establishment of barrier properties in the intraretinal vessels, the partial normalization of the proliferative vessels, and the abnormalities that persist. It is suggested that the vascular changes occur in successive stages: closure and obliteration during hyperoxia, vasoproliferation induced by hypoxia, and normalization after the relief of hypoxia with distinct cellular mechanisms and stimuli. It is argued that the same stages can be seen in the human form of ROP; two possible stimuli for the fibroplasia that damages the retina in human ROP are discussed.
本研究记录了猫科动物早产儿视网膜病变（ROP）过程中视网膜血管系统的变化。作者描述了在高氧环境下视网膜血管的闭合和闭塞、增殖性血管生长的模式和速度（动物回到室内空气环境后，增殖性血管从视盘以壮观的“玫瑰花结”模式延伸）、视网膜前血管生长的形成以及新血管最初缺乏屏障特性。最后，报告了血管系统对缺氧缓解的反应，包括视网膜内血管屏障特性的逐渐建立、增殖性血管的部分正常化以及持续存在的异常情况。研究表明，血管变化分连续阶段发生：高氧期间的闭合和闭塞、缺氧诱导的血管增殖以及缺氧缓解后的正常化，各阶段具有不同的细胞机制和刺激因素。有人认为，人类形式的ROP也可见到相同阶段；文中讨论了人类ROP中损害视网膜的纤维增生的两种可能刺激因素。
