| Objective: Proliferative vitreoretinopathy (PVR) is one of serious ocular disorders that lead to visually impaired and even blindness. Diseases such as rhegmatogenous retinal detachment, ocular trauma and diabetic retinopathy are main causation. That excessive proliferation of retina pigment epithelial and neural glial cells et,form fiber membrane proliferation behind the vitreous and on the surface of retina, that contract widely to lead traction retina detachment. Proliferate intraocular fibrous lead to traction retina detachment after perforating trauma, that call traumatic PVR. it's basic pathological feature is that cells migrate into vitreous and surface of retina to proliferate.At present, although surgery is an effective method that removes membrane proliferation of PVR, it's high Recurrence rate and damage blood-retinal barrier or blood-aqueous barrier. That result to serious inflammation and high recurrence. So far, many researching drugs that reported have great toxicity or short half-life. Therefore, we need drugs that against short half-life and non-toxicity prevent PVR.Suramin can interfere with the binding of growth factors and cell factors that inhibits proliferation and transition of RPE cells and participates cell signal transduction. Recently, there have considerable research that suramin inhibit cultivation RPE cells in vitro and non report that suramin prevent traumatic PVR at home and abroad.This experiment want to build a feasible traumatic PVR module of rabbit that injecting PRP and different concentrations suramin into vitreous. We can observe pathological changes of fundus oculi and eye with ophthalmoscope (OPh) and light microscope respectively of experimental traumatic PVR model rabbit and measuring the changes of epidermal growth factor and tumor necrosis factor in corpus vitreous and eye B-scan of the model rabbit eye to discuss preventing mechanism ,to provide the theoretic foundation for the application in clinic.Methods: forty Newzerland white rabbits that are 2-2.5kg in weight and sex undiscriminating were selected randomly .they ere divided randomly into five groups on average. traumatic PVR models were induced in rabbits by intravitreal injection of Platelet rich Plasma, The eyes received an intravitreal injection of saline(0.1ml) or suramin(0.1ml) in doses of 40mg/ml,60mg/ml and 80mg/ml, the blank group received nothing. After surgery, the eyes were examined ophthalmoscopically on the 1st, 3rd, 5th, 7th, 10th, 14th, 21st, 28th days and the stage of proliferative vitreoretinopathy was evaluated, Funduscope and BUS. The rabbits were taken out vitreous body, and the wiped off cornea and crystal in anaesthesia on 28th. To observe pathological changes of the retina, the content of EGF and TNF-αwas measured by ELISA and RIA. SPSS13.0 was used to process all dates.Result: 1. Observing pathological changes of fundus oculi and eye with ophthalmoscope (OPh) and light microscope and recording grades on fastenberg. Hyperplasia level of vitreous body and retina in different time by silt lamp microscope, funduscope: After surgery, there was not different significantly between experiment group 1, 2, 3and model group on the 1st, 3rd, 7th days, but the development was slow. Average level of experiment group 1,2,3 were lower than model group on 14th, 21st, 28th day, there was significantly statistical significance(P>0.05). experiment group 2, 3 were lower than group1 (P<0.05), and there was not significant difference between experiment group 2 and experiment group 3 (P > 0.05). Histological analysis revealed no significant functional changes.2. Contents of TNF-αand EGF of vitreous compared with five groups on 28 days. Compared with model group, the contents of TNF-αand EGF were decreased greatly significantly change in the experiment groups (P < 0.01). There was significantly change when compared with the content of TNF-αin blank group(P<0.01or P<0.05), While the levels of EGF in the experiment group 2 and 3 were not different significantly compared with blank group(P>0.05). The contents of TNF-αand EGF in the experiment group 2 and 3 was significantly compared with experiment 1(P<0.01or P<0.05). But there was no significant between experiment group 2and 3 (P>0.05).3. BUS: Normal group: the vitreous body was transparent and not abnormity echo; on the 1st, 3rd day, model and experimental groups: finding out of varying digrees dot-shaped, floc and small band echo in vitreous body, that doesn't closely link with eye ball wall; on the 7th, model and experiment groups: showing uneven, different length and traveling irregular echo or bending and forks, a single contact with eye ball wall and significant backward movement, and sporting obviously in vitreous body. On the 14th day, model group: finding out of facula of mezzo forte echo of wadding, thick and strip shape and jointing with optic pallar. Experiment group: finding out of facula of mezzo forte echo of dot and strip shape and not jointing with eyeball, and sporting obviously in vitreous body. On the 21st day, model group: finding out of facula of assembling flaky mezzo forte echo and light strap of strong echo of arc and strip shape, and singly jointing with eyeball obviously in vitreous body, experiment group: finding out facula of mezzo forte echo of irregular shape, and not jointing with eyeball and sporting obviously.On the 28th day, model group: fining out strong echo of irregular arc and strip shape, that show"V"or"Y"shapes and lie in the disc and jointing with jagged edge bilaterally in vitreous body. Experiment group : finding out light strap of mezzo forte echo of uneven, and irregular shape, and not jointing with eyeball and sporting obviously in vitreous body.Conclusion: 1. With the extension of times, the proliferation degrees of model group of PVR develop more serious grades. While suramin experiment groups obviously decrease with the increasing concentraion. So, the role that suramin inhibit traumatic PVR correlate on time and concentration.2. The content of TNF-αand EGF in vitreous of model group obviously below suramin group .it show that factors play an important role in mechanism of traumatic PVR ,suramin can effectively inhibit the developing of traumatic PVR.3. Histology reveal that injecting suramin into vitreous is effective, safe and long half-life, and have less side effect.
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