苏拉明抑制兔外伤性增生性玻璃体视网膜病变的实验性研究
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摘要
目的:增生性玻璃体视网膜病变(proliferative vitreo- retinopathy,PVR)是引起视力障碍甚至失明的严重眼病之一。孔源性视网膜脱离、眼外伤、糖尿病视网膜病变等疾病是造成PVR的主要原因。PVR是由于视网膜色素上皮细胞(retina pigment epithelial cells, RPE cells)和神经胶质细胞等的过度增生,在玻璃体后面和视网膜表面形成纤维增殖膜,纤维膜广泛收缩可造成牵拉性视网膜脱离(traction retina detachment, TRD)。如果TRD是由于眼球穿通伤后眼内纤维组织过度增生而引起,则称之为外伤性PVR,其是以细胞迁移进入玻璃体和视网膜表面进行增生为基本病理特征。
目前,手术治疗虽可有效去除PVR增生膜,但同时也破坏了血-视网膜屏障、血-房水屏障,结果炎症反应重,复发率高。寻求有效的药物辅助治疗是目前研究的方向。虽然已有抗PVR药物的研究报道,但这些药物毒副作用比较大或半衰期比较短,因此,寻求对眼组织无毒副作用和半衰期长的药物来防治PVR具有重要的临床意义。苏拉明具有抑制RPE细胞和神经胶质细胞增生和移行,并参与细胞信号传导的作用。近年,国内外对苏拉明抑制体外培养的RPE细胞的研究已有报道,但对防治外伤性PVR的研究尚未见报道。本实验通过采用自体富含血小板血浆玻璃体腔注射,创建一种可行的兔外伤性PVR模型,同时玻璃体腔内注射不同浓度苏拉明。采用双抗夹心ELISA法和放射免疫方法分别检测五组玻璃体液中EGF和TNF-α的含量,观察外伤性PVR模型组和实验组中眼底和视网膜病理的改变,从而探讨苏拉明防治PVR的作用机制,为将来临床应用提供理论依据。
方法:选用健康新西兰大白兔40只,雌雄兼用,体重2.5～3.2kg。采用富含血小板血浆玻璃体腔注射制备兔PVR模型,随机抽取8只作为空白组,其余36只制备外伤性PVR模型,并随机分为4组,每组8只。分别为模型组:玻璃体腔内一次性注入0.1ml生理盐水;实验1、2、3组:玻璃体腔内一次性注入0.1ml浓度分别为40mg/ml、60mg/ml和80mg/ml苏拉明。分别于术后第1、3、7、14、21、28天在充分散瞳下用裂隙灯显微镜和直接检眼镜观察并记录伤口、角膜、前房及玻璃体视网膜的改变,参照Fastenberg评级标准进行分级,并进行眼底照相及眼B超检查,采用双抗夹心ELISA法和放射免疫方法分别检测玻璃体液中EGF和TNF-α的含量。实验数据采用SPSS13.0统计软件包进行统计分析,PVR分级情况采用秩和检验,P<0.05作为显著标准。抽取玻璃体标本后立即摘除眼球,取伤口附近视网膜组织标本常规进行HE染色、显微镜观察和照相。
结果:1.用裂隙灯显微镜、眼底镜观察玻璃体视网膜改变,并按Fastenberg评级标准记录。第1、3、7天时实验1、2、3组玻璃体视网膜增生相对较缓慢,其增生级别与模型组比较,统计上无显著性差异(P>0.05)。术后第14天,实验3组的增生级别明显低于模型组,两者比较有显著性差异(秩和检验P<0.05),其余组之间无显著性差异。术后21、28天实验1、2、3组的平均增生级别均低于模型组,与模型组比较有显著性差异(秩和检验P<0.05)。实验2、3组的平均增生级别低于实验1组,与实验1组比较有显著性差异(秩和检验P<0.05)。实验2、3组之间比较无显著性差异(秩和检验P>0.05)。组织学检查,苏拉明实验三组均未发现明显的视网膜形态改变。
2.第28天,五组玻璃体中TNF-α和EGF含量进行比较。实验1、2、3组玻璃体腔中TNF-α和EGF含量均低于模型组,有极显著性差异(P<0.01)。实验1、2、3组玻璃体腔中TNF-α的含量均高于空白组,有显著性差异(P<0.01或p<0.05)。实验1组玻璃体腔中EGF的含量高于空白组,有极显著性差异(P<0.01)。实验2、3组玻璃体腔中EGF的含量与空白组无显著性差异(P>0.05)。实验2、3组玻璃体腔中TNF-α和EGF含量均低于实验1组,有显著性差异(P<0.01或P<0.05)。实验2、3组间玻璃体腔中TNF-α和EGF含量无显著性差异(P>0.05)。
3. B超结果:第1、3天,模型组及实验组:玻璃体内不同程度的斑点状、絮状或细带状回声,未与球壁回声紧密相连。第7天,模型组及实验组:表现为不均匀的、长短不一、走行不规则的回声带,或与其平行、弯曲,与球壁单一接触时有明显后运动,有多个粘连点时后运动不显著,大多不与视乳头连接。第14天,模型组:玻璃体内不同形状较粗条带状中强回声,与视乳头相连;实验组:玻璃体腔内可探及形态不规则的中强回声光斑,不与眼球壁相连,有明显的后运动。第21天,模型组:玻璃体腔内可探及聚集成片的强回声光斑及条状强回声光带,与眼球壁单一接触的有明显后运动;实验组:玻璃体内见块状或膜状回声及少量带状回声,少量走行不规则回声带,不与眼球壁相连,有明显后运动。第28天,模型组:玻璃体内弧形带状强回声,与球壁相连或与视乳头相连的条带,转动眼球时,光带轻度震颤或呈“V”形脱离尖端位于视乳头区,两端连于两侧锯齿缘;实验组:玻璃体腔内可探及不均匀的中强回声光带,不与眼球壁相连。
结论:1.随着时间延长,PVR模型组的增生程度发展至更严重等级;苏拉明实验组的增生程度随着浓度的增加而显著性降低。说明苏拉明对外伤性PVR的抑制作用与时间及浓度有关;
2.苏拉明实验组玻璃体腔内EGF、TNF-α的含量显著性低于模型组;说明细胞因子在外伤性PVR发病机制中起着重要作用,同时苏拉明能有效抑制兔外伤性PVR的发生和发展;
3.形态学表现说明苏拉明玻璃体腔内注射安全,维持药效时间长,对视网膜无明显毒副作用。
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.
目前,手术治疗虽可有效去除PVR增生膜,但同时也破坏了血-视网膜屏障、血-房水屏障,结果炎症反应重,复发率高。寻求有效的药物辅助治疗是目前研究的方向。虽然已有抗PVR药物的研究报道,但这些药物毒副作用比较大或半衰期比较短,因此,寻求对眼组织无毒副作用和半衰期长的药物来防治PVR具有重要的临床意义。苏拉明具有抑制RPE细胞和神经胶质细胞增生和移行,并参与细胞信号传导的作用。近年,国内外对苏拉明抑制体外培养的RPE细胞的研究已有报道,但对防治外伤性PVR的研究尚未见报道。本实验通过采用自体富含血小板血浆玻璃体腔注射,创建一种可行的兔外伤性PVR模型,同时玻璃体腔内注射不同浓度苏拉明。采用双抗夹心ELISA法和放射免疫方法分别检测五组玻璃体液中EGF和TNF-α的含量,观察外伤性PVR模型组和实验组中眼底和视网膜病理的改变,从而探讨苏拉明防治PVR的作用机制,为将来临床应用提供理论依据。
方法:选用健康新西兰大白兔40只,雌雄兼用,体重2.5～3.2kg。采用富含血小板血浆玻璃体腔注射制备兔PVR模型,随机抽取8只作为空白组,其余36只制备外伤性PVR模型,并随机分为4组,每组8只。分别为模型组:玻璃体腔内一次性注入0.1ml生理盐水;实验1、2、3组:玻璃体腔内一次性注入0.1ml浓度分别为40mg/ml、60mg/ml和80mg/ml苏拉明。分别于术后第1、3、7、14、21、28天在充分散瞳下用裂隙灯显微镜和直接检眼镜观察并记录伤口、角膜、前房及玻璃体视网膜的改变,参照Fastenberg评级标准进行分级,并进行眼底照相及眼B超检查,采用双抗夹心ELISA法和放射免疫方法分别检测玻璃体液中EGF和TNF-α的含量。实验数据采用SPSS13.0统计软件包进行统计分析,PVR分级情况采用秩和检验,P<0.05作为显著标准。抽取玻璃体标本后立即摘除眼球,取伤口附近视网膜组织标本常规进行HE染色、显微镜观察和照相。
结果:1.用裂隙灯显微镜、眼底镜观察玻璃体视网膜改变,并按Fastenberg评级标准记录。第1、3、7天时实验1、2、3组玻璃体视网膜增生相对较缓慢,其增生级别与模型组比较,统计上无显著性差异(P>0.05)。术后第14天,实验3组的增生级别明显低于模型组,两者比较有显著性差异(秩和检验P<0.05),其余组之间无显著性差异。术后21、28天实验1、2、3组的平均增生级别均低于模型组,与模型组比较有显著性差异(秩和检验P<0.05)。实验2、3组的平均增生级别低于实验1组,与实验1组比较有显著性差异(秩和检验P<0.05)。实验2、3组之间比较无显著性差异(秩和检验P>0.05)。组织学检查,苏拉明实验三组均未发现明显的视网膜形态改变。
2.第28天,五组玻璃体中TNF-α和EGF含量进行比较。实验1、2、3组玻璃体腔中TNF-α和EGF含量均低于模型组,有极显著性差异(P<0.01)。实验1、2、3组玻璃体腔中TNF-α的含量均高于空白组,有显著性差异(P<0.01或p<0.05)。实验1组玻璃体腔中EGF的含量高于空白组,有极显著性差异(P<0.01)。实验2、3组玻璃体腔中EGF的含量与空白组无显著性差异(P>0.05)。实验2、3组玻璃体腔中TNF-α和EGF含量均低于实验1组,有显著性差异(P<0.01或P<0.05)。实验2、3组间玻璃体腔中TNF-α和EGF含量无显著性差异(P>0.05)。
3. B超结果:第1、3天,模型组及实验组:玻璃体内不同程度的斑点状、絮状或细带状回声,未与球壁回声紧密相连。第7天,模型组及实验组:表现为不均匀的、长短不一、走行不规则的回声带,或与其平行、弯曲,与球壁单一接触时有明显后运动,有多个粘连点时后运动不显著,大多不与视乳头连接。第14天,模型组:玻璃体内不同形状较粗条带状中强回声,与视乳头相连;实验组:玻璃体腔内可探及形态不规则的中强回声光斑,不与眼球壁相连,有明显的后运动。第21天,模型组:玻璃体腔内可探及聚集成片的强回声光斑及条状强回声光带,与眼球壁单一接触的有明显后运动;实验组:玻璃体内见块状或膜状回声及少量带状回声,少量走行不规则回声带,不与眼球壁相连,有明显后运动。第28天,模型组:玻璃体内弧形带状强回声,与球壁相连或与视乳头相连的条带,转动眼球时,光带轻度震颤或呈“V”形脱离尖端位于视乳头区,两端连于两侧锯齿缘;实验组:玻璃体腔内可探及不均匀的中强回声光带,不与眼球壁相连。
结论:1.随着时间延长,PVR模型组的增生程度发展至更严重等级;苏拉明实验组的增生程度随着浓度的增加而显著性降低。说明苏拉明对外伤性PVR的抑制作用与时间及浓度有关;
2.苏拉明实验组玻璃体腔内EGF、TNF-α的含量显著性低于模型组;说明细胞因子在外伤性PVR发病机制中起着重要作用,同时苏拉明能有效抑制兔外伤性PVR的发生和发展;
3.形态学表现说明苏拉明玻璃体腔内注射安全,维持药效时间长,对视网膜无明显毒副作用。
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.
引文
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3 陈洁等.吲哚美辛防治 PVR 的实验性研究[J]. 中国中医眼科杂志,2006, 9(4):150-156
4 Holger Mietz, et al. Decorin and suramin inhibit ocular fibroblast collagen production[J]. BrJ Ophthalmol ,1995,79:874-882
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6 朱晓波,唐仕波,蔡葵花,等. 双波长等吸收紫外分光法测定玻璃体内苏拉明质量浓度[J]. 中山大学学报医学科学版, 2004,25(3):225-230
7 姜彩辉,张卯年.实验性外伤性增生性玻璃体视网膜病变动物模型的改进.眼科研究,2003,21(6):579-581
8 Fastenberg DM,Diddie KR, Dorey K, et al. the role cellular proliferation in an experimental model of massive periretinal proliferation.Am J Ophthalmol, 1982,93:565-572
9 张秀兰, 吕林, 高汝龙 牵引性视网膜脱离[J]国外医学·眼科分册, 1993, 17: 361-364
10 Baudouin C, Kho srzvi E, P isella PJ , et al. Inflammation measurement and immunocharacterization of cell proliferation in an experimental model of proliferative vitreoretinopathy[J].Ophthalmic Res, 1998, 30: 340
11 Proliferative vitreoretinopathy: an overview [J]. Surv Ophthalmol, 1998, 43(1):3-18.
12 Leshey KH, Hackett S F , Singer J H , Campochiaro PA. growth factor responsive hess of human pigment epithelial cells [J].Invest Ophthalmol Vis Sci ,1990;31( 5): 839-846.
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2 郑燕林,王毅等。水蛭素对实验性外伤性 PVR 形成的抑制作用[J].中国中医眼科杂志 2000, 9(20):120-124
3 陈洁等.吲哚美辛防治 PVR 的实验性研究[J]. 中国中医眼科杂志,2006, 9(4):150-156
4 Holger Mietz, et al. Decorin and suramin inhibit ocular fibroblast collagen production[J]. BrJ Ophthalmol ,1995,79:874-882
5 Sporn M Roberts. A Gand book of experimental Phaomacology Vol95/I PePtide growth factor sand their rcetors 1. Berlm: Sing Verlay, 1990, 18:168-175
6 朱晓波,唐仕波,蔡葵花,等. 双波长等吸收紫外分光法测定玻璃体内苏拉明质量浓度[J]. 中山大学学报医学科学版, 2004,25(3):225-230
7 姜彩辉,张卯年.实验性外伤性增生性玻璃体视网膜病变动物模型的改进.眼科研究,2003,21(6):579-581
8 Fastenberg DM,Diddie KR, Dorey K, et al. the role cellular proliferation in an experimental model of massive periretinal proliferation.Am J Ophthalmol, 1982,93:565-572
9 张秀兰, 吕林, 高汝龙 牵引性视网膜脱离[J]国外医学·眼科分册, 1993, 17: 361-364
10 Baudouin C, Kho srzvi E, P isella PJ , et al. Inflammation measurement and immunocharacterization of cell proliferation in an experimental model of proliferative vitreoretinopathy[J].Ophthalmic Res, 1998, 30: 340
11 Proliferative vitreoretinopathy: an overview [J]. Surv Ophthalmol, 1998, 43(1):3-18.
12 Leshey KH, Hackett S F , Singer J H , Campochiaro PA. growth factor responsive hess of human pigment epithelial cells [J].Invest Ophthalmol Vis Sci ,1990;31( 5): 839-846.
13 王景文,王桂云等.增生性玻璃体视网膜病变玻璃体中EGF 的含量[J] .中国航天工业医药,1999,6(2):11-13
14 惠延年.国际增生性玻璃体视网膜病变讨论会[J] .国际医学眼科分册,1989,13(2):103-106
15 蔡季平, 周韵秋, 奚寿增. 生长因子对神经胶质细胞增殖的作用[J] . 中华眼底病杂志,1998,14(1): 33-34
16 Jin M, He S, Worpel V , et al. Promotion of adhesion and migration of RPE cells to provisional extra cellular matrices by TNF-αlpha [J] . Invest Ophthalmol Vis Sci, 2000, 41(13): 4324 - 4332
17 Braddok PS, Hu DE, Fan PD, et al. A structure activity analysis of antagonism of the growth factor and antigenic activity of basic fibroblast growth factor by suramin and related polyanions [J] .Br J Cancer, 1994,69 (5):890-898
18 Bemardini N, Giannessi F, Bianchi F, et al. Involvement of basic fibroblast growth factor in suramin-induced inhibition of V79/AP4 fibroblast cell proliferation [J]. Br J Cancer, 1993,67 (6):1209-1216
19 Voogd TE, V ansterkenburg EL, Wilting J, et al. Recentre-search on the biological activity of suramin [J]. P harmacol Rev,1993; 45 (2):177-203
20 De Souza OF, Sakamoto T, Kimura H, et al. Inhibition of experimental proliferative vitreoretinopathy in rabbits by suramin [J]. Ophthalmologica,1995,209:212-216
21 Leschey KHHines J, Singer JH et al inhibition of growth factor effects in retinal pigment epithelial cells[J] . Invest Ophthalmol Vis Sci, 1991, 32(6):4311-4316
22 朱晓波,唐仕波等 苏拉明对碱性成纤维细胞因子促进RPE 细胞增殖作用拮抗效应研究[J].中华眼科杂志,200541(2):110-113
23 Cleary PE. Ryan SJ. experimental Posterior Penetrating eye injury in the Rabbit. I method of Production and natural history.Br J OPhthalmol,1979,63(5):306-311
24 Sugiat G, Tano Y, MaehemerR, et al. Intraviteral autotransplantation of fibroblasts. Am JOPhthalmol, 1980, 89: 121-130
25 Meredith TA, Fieker L, Stevens R, et al. Suppression of experimental tractional retinal detachment by low-dose radiation therapy. Arch Ophthalmol, 1988, 106: 673-675
26 Hui YN Sorgenet NRyanSJ. Posterior vitreous Seperation and detachment induced by macrophages.Graefes Arch Clin Exp Ophthalmol, 1987, 225(4): 279-284
27 Yeo JH, Sadeghi J, CamPoehiaro PA, et al. Intravitreous fibronection and platelet-derived growth factor. new model of retraction retinal detachment. Arch Ophthalmol, 1986, 104(3): 417-421
28 Pisella PJ, BandouinC. Stages of cell Proliefration in an experimental model of vitreoretinal Proliefration following injection of Platelet-rich Plasma.J Fr Ophthalmol, 1996, 19(10): 576-584
1 The retina society terminology committee. The classification of retinal detachment with proliferative vitreo retinopathy[J]. Ophthalmology, 1983, 90: 121-125
2 张国明,高汝龙. 关于增生性玻璃体视网膜病变命名和分类的看法[J] .临床眼科杂志,2004 ,12(4):378-380
3 Lean JS, Stern WH, Irvine AR. Classification of proliferative vitreoretinopathy used in the silicone study[J]. Ophthalmology, 1989, 96: 765-771
4 Machemer R, A aberg TM, F reeman HM. An updated classification of retinal detachment with proliferative vitreoretinopathy[J].Am J Ophthalmol, 1991, 112: 159-165
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