ABSTRACT
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
ABSTRACT
Objective To study the changes in the activity of two important enzymes related to the productivity of aqueous humor, namely Na +-K +ATPase and carbonic anhydrase, and to probe further into the mechanism of induction of chronic ocular hypotony by traumatic anterior proliferative vitreoretinopathy. Methods A rabbit model of chronic hypotony induced by traumatic anterior proliferative vitreoretinopathy was reproduced. At the 2nd , 4th, 8th and 16th week after trauma, IOP was measured. Then eyeballs were removed, and a part of ciliary body was harvested for orthodox pathological section and HE staining, and another part of ciliary body was used for determination of Na +-K +ATPase's activity and histochemical assessment of carbonic anhydrase. Result Activity of Na, K-ATPase decreased gradually in the experimental group, but there is no remarkable change in the control group, and the difference was significant. In the experimental group, the activity of carbonic anhydrase was nearly normal, but the activity of carbonic anhydrase in the area of injured epithelium was low, and it was similar to the control. Conclusion Activity of ciliary Na +-K +-ATPase and carbonic anhydrase decrease in activity after traumatic anterior proliferative vitreoretinopathy, which is an important causative factor of chronic hypotony.