外伤性aPVR引起慢性低眼压的发病机制探讨

目的探讨外伤性前部增生性玻璃体视网膜病变(aPVR)病理状态下低眼压的发生、发展及转归，为防治外伤性aPVR引起的慢性低眼压提供理论依据。方法利用青紫兰兔制作外伤性aPVR引起慢性低眼压的动物模型(n=8)，于术前及术后不同时间点分别观测眼压(IOP)，并行光镜及电镜观察。结果术后1周、2周、4周、8周实验组平均眼压明显低于对照组(P＜O．01)。光镜检查发现实验组术后2周、4周、8周睫状体水肿，术后4周及8周睫状体无色素上皮萎缩、缺失。电镜检查发现实验组术后4周和8周睫状体无色素上皮线粒体明显减少，细胞内空泡。结论外伤性aPVR睫状膜的增生和收缩引起对睫状上皮的牵拉，造成睫状体无色素上皮萎缩和睫状体水肿，进而促进慢性低眼压的发生。

Study on pathogenesis of chronic hypotony following traumatic anterior proliferative vitreoretinopathy

Objective To study the occurrence, development and outcome of hypotony following traumatic anterior proliferative vitreoretinopathy (aPVR), so as to provide a theoretical basis for its prevention and treatment. Methods An animal model of chronic hypotony following traumatic aPVR was reproduced in rabbits. The intraocular pressure (IOP) was measured before the experiment and on days 7, 14, 28 and 56 after the injury. Rabbits were killed on days 14, 28 and 56 after the experiment, prepared for pathological and ultrastructure examination. Results The average IOP of experimental group was significantly lower than that of control group on days 7, 14, 28 and 56 (p<0.01). Microscopic examination showed edema of the ciliary body on days 14, 28 and 56, and atrophy or absence of the non-pigmented ciliary epithelium on days 28 and 56 postinjury in experimental group. Electronic microscopic examination showed that the amount of mitochondria was decreased, and there were many vacuoles in the non-pigmented ciliary epithelium in the experimental group four and eight weeks after the injury. Conclusions The epiciliary membrane in traumatic aPVR dragged the ciliary body by its hyberplasia and contraction, giving rise to atrophy of non-pigmented epithelium and edema of ciliary body, further aggravating hypotony.