目的　探讨前部增生性玻璃体视网膜病变 (anterior proliferative vitreoretinopathy,a PVR)病理状态下低眼压的发生、发展及转归 ,为防治 a PVR引起的慢性低眼压提供理论依据。　方法　利用培养的同种兔皮肤成纤维细胞制作 a PVR引起慢性低眼压的动物模型 ,于术前及术后不同时间点分别观测眼压(intraocular pressure,IOP) ,行超声生物显微镜 (ultrasound biomicroscopy,U BM)检查 ,并做病理、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<0 .0 1)。 UBM显示术后 4周实验组虹膜后睫状体内侧条形回声 ,术后 4周及 8周实验组周边视网膜牵引性脱离。光镜检查发现实验组 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　在 a PVR病理状态下 ,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 ,可能是引起慢性低眼压的主要原因。 Objective To investigate the occurrence, development and prognosis of hypothalamic pressure in anterior proliferative vitreoretinopathy (a PVR) in order to provide a theoretical basis for prevention and treatment of chronic hypotony caused by PVR. Methods Animal models of chronic low intraocular pressure induced by a PVR were made in the same kind of rabbit skin fibroblasts. Intraocular pressure (IOP) was observed before and after surgery. Ultrasound biomicroscopy , U BM) examination, and pathology, electron microscopy. Results The average intraocular pressure (IOP) of the experimental group at 1 week, 2 weeks, 4 weeks and 8 weeks after operation was significantly lower than that of the control group (P <0.01). UBM showed four weeks after surgery in the experimental group, the inner iris ciliary body after the strip echo, 4 weeks and 8 weeks after the experimental group peripheral retinal traction detached. Light microscopy examination found that the experimental group 4 weeks and 8 weeks ciliary body ametropic atrophy, missing. Electron microscopy examination found that the experimental group 4 weeks and 8 weeks after ciliary body no pigment epithelial mitochondria significantly reduced intracellular vacuolar. Conclusions In a PVR pathology, the proliferation and contraction of the ciliary membrane cause ciliary epithelial traction, resulting in atrophy of the ciliary body without pigment epithelium, which may be the main cause of chronic hypotony.