Experimental Study On Chronic Hypotony Induced By Severe Ocular Trauma

Objective :To investigate the occurrence, progress, and the mechanism of chronic hypotony induced by severe ocular trauma through animal model.Methods:20 adult pigmented rabbits were randomly selected into two groups.32 eyes of 16 rabbits were selected for the group 1 and the other 8 eyes of 4 rabbit were selected for the group 2.In the group 1,one eye of all the rabbits was considered as experimental group and the other as experimental control group,In the group 2, both eyes of all the rabbits were considered as blank control group. In experimental group, we removed the lens nucleus and parts of the cortices through a corneal limbal incision, and cut the iris and ciliary body Radially at 1 and 7 o'clock until the blood flow out, then break the capsule with a discussion needle, and blended the Blood,capsule Pieces, remaining lens cortices with he vitreous near the ciliary body. In experimental control group, we only removed the lens by ECCE. No treatment was conducted in blank control group. The intraocular pressure (IOP) and the concentration of PGE₂ in aqueous humor was measured on 1 day,1 week,2 weeks,4 weeks and 8 weeks after surgery. At weeks 2,4,8,The examinations of Ultrasound biomicroscopy(UBM), light microscopy, electron microscopy were made at weeks 2,4,8, as well as the determination of Activity of Na⁺, K⁺-ATPase in ciliary body.Results:The mean IOP of experimental group was evident lower than that of control group at weeks 2,4 and 8(p<0.01).All the eyes of experimental group had an IOP less than 5 mmHg at week 8 and a mean of 3.5 mmHg. The mean IOP of experimental control group is 13.2 mmHg at week 8. UBM showed the pattern of dots and cords in anterior vitreous in experimental group at 2 weeks after surgery, the cordlike echoes increased and enhanced at weeks 4, 8. PGE2 concentration in aqueous in experimental group was apparently higher than that in experimental control and blank control group (P<0. 05) until 4th week postoperative. Activity of Na⁺,K⁺-ATPase in ciliary body decreased gradually in the experimental group, and was apparently lower than that in experimental control and blank control group (P<0.05).Light microscopic showed there were proliferated fibriform matters among ciliary precesses of the experimental group, some non-pigmented ciliary epithelium atrophied or disappeared. Electronic microscopy showed mitochondria swelling, mitochondrial cristae disappearing, endoplasmic reticulum dilating, and intercellular space was enlarged in ciliary epithelium in experimental group, there were many vacuoles in the non-pigmented ciliary epithelium, some non-pigmented ciliary epitheliumdisappeared.Conclusions:This method of establishing chronic hypotony model after ocular trauma hashigh success rate. Chronic ocular hypotony cause the damage of the retinal structure.The chronic ocular hypotony after trauma is associated with the occurrence of aPVR and thedecrease in Na⁺,K⁺-ATPase activity in ciliary body. The persistent higher PGE₂ concentration inaqueous might be another factor in chronic hypotony after ocular trauma.