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BackgroundAnterior proliferative vitreoretinopathy (aPVR)is a tissue injury and repair progress,and treatment of aPVR is very important in clinic.Chitosan drug delivery system is becoming a hot spot for its large lading dose and long acting duration.ObjectiveThe present study was to investigate the curative effect of a triamcinolone acetonide (TA) drug delivery system after implantation into the suprachoroidal space to treat traumatic aPVR.MethodsaPVR models were created in the left eyes of 65 healthy pigment rabbits by performinga 5 mm penetrating incision 2.5 mm posterior to limbum at 10:30-11:30.The animals were randomly divided into 4groups.Blank chitosan was implanted into the suprachoroidal space as the blank control group.Chitosan with 1 mg TA was implanted in the TA + chitosa group.The TA solution ( containing 1 mg TA) was intravitreally injected in the TA injection group.Fifteen models were used as the traumatic control group.Another 15 left eyes of normal pigment rabbits were used as the normal control group.The thickness of the ciliary tissue was measured using a ultrasound biomicroscope(UBM) 3,5 and 8 weeks after operation.The animals were sacrificed by excessive anesthesia and eyeballswereobtainedforhistopathologicalandultrastructuralexaminations.ResultsHistopathological examination showed the edema of the ciliary tissue and inflammatory cells infiltration in the blank control group,TA injection group and model control group,but mild response was seen in the TA + chitosa group.Severe damage in the ciliary tissue and subcellular organelle was found in the blank and model control groups,but mild damage was detected in the TA + chitosa group under the transmission electron microscope.UBM examination revealed that obvious abnormalities were visible in the ciliary and iris tissue in the blank control group,TA injection group and traumatic control group,but a mild abnormality was seen in the TA + chitosa group.Significant differences in ciliary thickness were exhibited among the 5 groups 2,5 and 8 weeks after operation (F =212.938,515.323,447.919,P＜0.01 ).Compared with the normal control group,ciliary thickness significantly increased in the blank control group and normal control group at various time points (all P＜0.05 ),but that in the TA + chitosa group was significantly lower than the normal control group at various time points ( two weeks:0.484±0.075 vs.0.327 ±0.094 ; five weeks:0.422 ±0.089vs.0.327±0.094 ;eight weeks:0.418±0.085 vs.0.327±0.094) (all P＞0.05). ConclusionsThe chitosan drug delivery system with TA suppresses the excessive proliferation of injured ocular tissue after implantation into the suprachoroidal space,which prevents the formation and development of aPVR.
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Objectives:To establish animal model of anterior proliferative vitreoretinopathy (aPVR) with cultured homologous dermal fibroblasts of rabbit, and to provide evidence why hypotony was caused by aPVR. Methods:Animal models of aPVR were established with cultured homologous dermal fibroblasts on pigmented rabbits. Rabbits were sacrificed on the 14th, 28th and 56th day after the operation to prepare naked eyes and to receive histological examinations. Results:Naked eye examination showed that the peripheral retina was detached by dragging in the experimental group 28 and 56 days postoperatively. Microscopic examination showed atrophy or absence of the non-pigmented ciliary epithelium on the 28th and 56th postoperative day in the experimental group. Conclusions:The epiciliary membrane in aPVR dragged the ciliary body, made atrophy of non-pigmented epithelium, which perhaps was the main cause of hypotony.
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Proliferative vitreoretinopathy is the principal cause of failure in rhegmatogenous retinal detachment surgery. The final cause of anatomic failure is anterior proliferative vitreoretinopathy. Surgical outcome of anterior proliferative vitreoretinopathy is poorer than that of posterior proliferative vitreoretinopathy. Of 147 cases which underwent vitreoretinal surgery from January through December 1993, 16 eyes(l6 patients) had anterior proliferative vitreoretinopathy. Seven eyes had anterior proliferative vitreoretinopathy at initial surgery(group 1). Remaining 9 eyes developed anterior proliferative vitreoretinopathy after primary vitrectomy(group 2). Of 16 eyes, 3 were aphakic, 2 were pseudophakic, and remaining 11 were phakic. Lens was removed in 11 phakic eyes. Meticulous vitreous base dissection and removal of anterior epiretinal membrane were performed. After minimal follow-up of 6 months, retina reattached in 11 eyes(69%) including all nine eyes of group 2. Nine eyes(56%) had postoperative visual acuity of 0.025 or better. These results suggest that both vitreous base dissection and meticulous removal of anterior and posterior epiretinal membrane should be crucial in improving surgical success rate of anterior proliferative vitreoretinopathy.
Subject(s)
Epiretinal Membrane , Follow-Up Studies , Retina , Retinal Detachment , Visual Acuity , Vitreoretinal Surgery , Vitreoretinopathy, ProliferativeABSTRACT
We reviewed the records of 23 patients who underwent repeat operation after initial vitreoretinal surgery in Chungnam National University Hospital between January 1993 and December 1993. Of 193 eyes who underwent vitreoretinal surgery in that period, 23(12%) had undergone reoperation. The most common cause of initial anatomic failure and reoperation was either new or recurrent proliferative vitreoretinopathy(10 eyes). Other causes included iatrogenic retinal tears(5 eyes), hidden retinal breaks(4 eyes), vitreous traction(1 eye), inappropriate chorioretinal adhesion(1 eye), and new break(1 eye). We performed vitreous base dissection on all 9 eyes with anterior proliferative vitreoretinopathy. With additional surgery and after a mean follow-up period of 10.4 months, 21(91%) of 23 retinas were reattached. The final cause of anatomic failure was anterior proliferative vitreoretinopathy. Of the 23 reoperated eyes, 20(87%) had postoperative visual acuity of 0.05 or better.
Subject(s)
Humans , Follow-Up Studies , Reoperation , Retina , Retinaldehyde , Visual Acuity , Vitreoretinal Surgery , Vitreoretinopathy, ProliferativeABSTRACT
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
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Objective To study the dynamics of aqueous humor in chronic hypotony induced by traumatic anterior proliferative vitreoretinopathy (aPVR), and to demonstrate physiologic mechanisms of the hypotony. Methods A model of hypotony to simulate traumatic aPVR was reproduced in rabbits. Preoperatively and on day 7, 14, 28 and 56 postoperatively, the aqueous humor flow rate and the uveoscleral outflow of aqueous humor were determined. Results The flow rate of aqueous humor in experimental group was reduced remarkably compared with that of control group on days 14, 28 and 56 (P
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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.