SOD和脂质过氧化反应在视网膜铜沉着症中的作用

测定了家兔眼球内铜异物伤后,视网膜中的抗氧化酶SOD活性和脂质过氧化反应产物MDA含量,以及玻璃体中铜离子浓度。SOD活性随玻璃体中铜离子浓度的升高而明显下降。7天时下降53.2%,4周时下降93.8%。MDA值在整个观察期间明显增高,最高达对照组的3倍,且与玻璃体中铜离子浓度的升高呈正相关。实验结果表明,脂质过氧化反应和视网膜SOD活性下降可能是眼铜质沉着症视网膜变性的重要因素之一。     

脂质过氧化与糖尿病性视功能损害

丙二醛(malondialdehyde,MDA)是脂质过氧化反应中的一种主要终产物,可以反映体内自由基和脂质过氧化活动的水平。我们测定了糖尿病患者的血清MDA,与正常对照组进行了比较,并同蓝色图形视觉诱发电位(Blue PatternVisual Evoked Potenfial;BP-VEP)进行了对比观察,探讨糖尿病患者体内脂质过氧化活动的水平及其与视网膜光感受器和视神经系统损害的关系。     

玻璃体出血对视网膜组织的脂质过氧化损伤

关于玻璃体出血是否引起视网膜损伤一直存在着争论。我们利用兔眼玻璃体出血模型,研究了视网膜脂质过氧化损伤。在玻璃体内注入0.2ml自体全血后,用硫代巴比妥酸荧光比色法测定视网膜内丙二醛含量。丙二醛是脂质过氧化的主要降解产物,在注血后10天达到0.166±0.087nmol/mg,明显高于对照眼(p<0.01)。透射电镜发现光感受器内、外节变性。本实验证实玻璃体出血对视网膜具有生化毒性。血红蛋白氧化和巨噬细胞产生的自由基作用,可能是富有脂质的视网膜损伤的重要原因,     

二硫化碳毒性视网膜损害的病理改变与脂质过氧化反应关系的实验研究

目的探讨CS2毒性视网膜损害的病理学改变与脂质过氧化反应的关系。方法对20只家兔实验性二硫化碳中毒所致的视网膜损害作视网膜组织的光镜、电镜观察和脂质过氧化反应的生化检测。结果视网膜超微结构：染毒兔视细胞变性,毛细血管内皮细胞囊样变。视网膜生化检测：染毒兔视网膜丙二醛活性增高（P＜0．05）,超氧化物歧化酶总活力降低（P＜0．05）。结论CS2对视网膜组织结构与功能的损害及视网膜脂质过氧化反应结果是一致的,其互为因果关系是可能的。     

二硫化碳毒性视网膜损害的病理改变与脂质过氧化反应关 …

目的 探讨ＣＳ２毒性视网膜损害的病理学改变与脂质过氧化反应的关系。方法 对２０只家兔实验性二硫化碳中毒所致的视网膜损害作视网膜组织的光镜，电镜观察和脂质过氧化反应的生化检测。结果 视网膜超微结构：染毒兔视细胞变性，毛细血管内皮细胞囊样变。视网膜生化检测；８染毒兔视网膜丙二醛活性增高，超氧化歧化酶总活力降低。     

氧化应激对小梁网的损伤

青光跟是一组以视网膜神经节细胞(RGCs)丢失和视野缺损为特征的神经退行性疾病,其病理机制尚不完全清楚,眼压升高被认为是青光眼发生和发展最主要的危险因素.小梁网及Schlemm管是房水引流系统的主要组成部分,其结构或功能异常可引起房水流出的受阻进而引起眼压升高.越来越多的证据表明,氧化损伤可能在人小梁网细胞凋亡、功能障碍及其他退行性改变过程中发挥作用.氧化损伤是体内氧化和抗氧化失衡,从而引起脂质过氧化反应、蛋白质变性、DNA损伤等一系列组织病理损伤的过程.既往研究发现青光眼患者房水中氧化应激标志物水平升高,且氧化应激可引起小梁网细胞DNA氧化损伤、细胞内线粒体氧化损伤和炎症反应.本文就氧化应激在小梁网功能损伤中发挥的作用及可能的机制进行综述.     

二硫化碳毒性视网膜功能损害与脂质过氧化反应关系的实验研究

为探讨二硫化碳毒性视网膜功能损害与脂质过氧化反应的关系，进行兔眼ERG生化检测。结果染毒3周后，染毒兔ERGb波振幅明显低于对照组，视网膜超氧化物歧化酶总活力（TSOD）较对照组降低，而MDA活性增高。ERGb波振幅与TSOD呈正相关而与MDA呈负相关。结论CS2毒性视网膜功能损害可能与脂质过氧化反应有关。     

兔角膜穿孔后房水内丙二醛的测定

兔角膜穿孔伤后,房水中丙二醛含量与正常相比显著增高,P<0.001。提示前房内发生了脂质过氧化反应。这一发现有助于对眼前节炎症反应的进一步认识。     

孔源性视网膜脱离视网膜下液丙二醛和锌,铜含量测定及临床意义

对８０例孔源性视网膜脱离患者视网膜下液及血清丙二醛、锌和铜水平进行了测定。结果表明：ＳＲＦ中有脂质过氧化毒性产物，其含量随ＲＲＤ眼瓿病变程度的加重而增加，并与ＳＲＦ中锌含量呈正相关。中度以上近视患者血清Ｃｕ／Ｚｎ比值显著高于正常人和低度近视患者（Ｐ≤０．０５）。锌、铜代谢异常和脂质过氧化毒性作用可能是ＲＲＤ发生和发展的病理因素之一。     

牛磺酸对大鼠视网膜光损伤的保护作用

视网膜光损伤是当前眼科临床工作中出现的—个新问题,它与老年性黄斑变性及drusen形成都有着密切关系。近来的研究表明,视网膜光损伤是由光照引起氧自由基产生而导致光化学反应,通过脂质过氧化反应造成膜系统的损伤。体外实验表明,牛磺酸可抑制蛙视杆细胞外段的脂质过氧化反应,减轻光对杆细胞外段的损伤。本文给大鼠腹腔注射牛磺酸,通过对视网膜电流图b波振幅变化的观察及组织学观察,试图验证牛磺酸对视网膜光损伤具有保护作用。     

Retinal dysfunction in cancer-associated retinopathy is improved by Ca(2+) antagonist administration and dark adaptation

PURPOSE: It was recently found that recoverin acts as an autoantigen recognized by sera of patients with cancer-associated retinopathy (CAR), and that CAR-like retinal dysfunction is produced by intravitreous administration of anti-recoverin antibody in Lewis rat eyes. To examine the pathologic molecular mechanism of CAR, and to elucidate an effective therapy for CAR, the function and morphology of CAR were compared with those of phototoxic retinal damage, another form of photoreceptor dysfunction, and the effect of nilvadipine, a Ca(2+) antagonist, on the retinal degenerations was studied, using these models. METHODS: Under different illumination conditions and/or medication with nilvadipine, the functional and morphologic properties of the retinas were evaluated after intravitreous injection of anti-recoverin antibody into Lewis rat eyes (six rats, 12 eyes in each experimental condition), using electroretinogram (ERG), rhodopsin phosphorylation, and light microscopy. RESULTS: Anti-recoverin antibody administered into the vitreous of Lewis rat eyes induced a significant decrease and increase of ERG responses and rhodopsin phosphorylation levels, respectively, under cyclic or continuous light. Similar changes were observed in eyes of rats bred under continuous illumination that did not receive anti-recoverin antibodies. However, anti-recoverin antibody-induced retinal dysfunctions were not observed in rat eyes under dark conditions. Administration of nilvadipine, a Ca(2+) antagonist, to the anti-recoverin antibody-treated rats and rats with phototoxic retinal dysfunction caused significant improvement of the deterioration of ERG and normalization of rhodopsin phosphorylation. CONCLUSIONS: The present data indicate that anti-recoverin antibody-induced retinal dysfunction was functionally similar to phototoxic retinal dysfunction and was markedly suppressed under dark conditions or by systemic administration of a Ca(2+) antagonist.     

Bright-flash electroretinography for the evaluation of eyes with opaque vitreous.

Standard retinal function tests are of limited value in assessing retinal function in eyes with opaque vitreous. We developed a method for obtaining an electroretinogram (ERG) from eyes with significant vitreous opacity by utilizing a much brighter than normal stimulating light. Of 115 eyes with vitreous opacities and good ERG responses to this bright-flash photostimulator, 47% would have been nonrecordable with a conventional ERG light source. Bright-flash ERG was often helpful in evaluating eyes with vitreous opacities for vitrectomy and was sometimes the only source of information regarding potential retinal function.     

视网膜电图对玻璃体出血机化和玻璃体手术的意义

报告118例(133眼)由各种疾病引起的玻璃体出血机化患者的视网膜电图(ERG)检查结果,其中31例作了玻璃体手术,结果表明,ERG检查对玻璃体出血机化的患者,能客观地反映其网膜功能,并对玻璃体手术的预后有指导作用。术前ERG检查,a、b波下降越严重,视功能损害显著,术后视力的预后越差,同时证实,玻璃体机化膜是影响a、b波波幅和时间的一个因素。     

Encapsulated cell-based intraocular delivery of ciliary neurotrophic factor in normal rabbit: dose-dependent effects on ERG and retinal histology

PURPOSE: ERG and histologic changes were investigated in normal rabbits after intravitreal implantation of encapsulated cell technology (ECT) devices releasing ciliary neurotrophic factor (CNTF). METHODS: Fifteen adult New Zealand White albino rabbits had ECT devices secreting CNTF at 22, 5, or 0 ng/d implanted in the superior temporal quadrant of the left eye. The low dose has been shown to produce substantial rescue of photoreceptors in the rcd1 canine model of retinal degeneration. Right eyes were untreated. Ganzfeld dark- and light-adapted ERGs and clinical observations were performed at 5, 15, and 25 days after implantation. Rod a-waves and rod and cone b-waves and outer nuclear layer (ONL) morphology were evaluated at 25 days. RESULTS: Clinical examination showed minimal changes in a few CNTF-treated eyes, including vitreous membranes and engorgement of iris vessels at day 25. Retinas appeared normal. CNTF did not significantly affect the rod a- or b-waves, although the b-wave amplitude tended to be larger in CNTF-treated retinas at low flash intensities. The cone b-wave amplitude was significantly reduced in high-dose eyes at some flash intensities. The ONL area in high-dose eyes was significantly greater because of increased thickness than in fellow retinas. ONL cell size was significantly increased, and staining density decreased in CNTF-treated retinas. CONCLUSIONS: CNTF, given by intravitreal ECT device at doses that protect photoreceptors in a canine model of retinal degeneration (5 ng/d), did not adversely affect either rod or cone ERG function of normal rabbit retina. The cone ERG was more sensitive to suppression being reduced, at low flash intensities, by 22 ng/d. Dose-related changes in the ONL and photoreceptor cell nuclei did not represent a toxic effect, because they were not associated with deficits in the rod ERG over a broad range of intensities.     

Preclinical investigation of fluorometholone acetate as a potential new adjuvant during vitreous surgery.

OBJECTIVE: To examine the effects of intravitreal fluorometholone acetate (FMT) on the morphology and function of the retina and to investigate its possible use for vitreous surgery. METHODS: Brown Norway rat eyes (n = 6, 12 groups) were injected with 0.05 ml of SF6 gas for vitrectomization. Four weeks later, FMT solution was injected into the vitreous cavity/subretinal space of the vitrectomized eyes at doses of 10, 20, and 40 mg/ml (0.05 ml/eye, n = 12 for each group). The retinal function was evaluated by electroretinography (ERG) at 4 and 8 weeks after FMT injection. Retinal toxicity was also assessed histologically by a light microscopy. Sham-operated eyes (0.05 ml of irrigating solution, n = 12) were used as control animals. FMT-assisted pars plana vitrectomy with internal limiting membrane (ILM) peeling was performed in primate eyes (n = 2). Retinal toxicity was assessed by ophthalmoscope, fluorescein angiography and electron microscopy three months after the vitreous surgery. RESULTS: There was no remarkable reduction in any ERG waves at either time interval at 4 and 8 weeks after the intravitreal/subretinal injection of FMT. No obvious histological change was observed in any of the rat eyes either. Using ophthalmoscope, fluorescein angiography and electron microscopy, the appearance of the primate retinas remained to be in a non-pathological condition. CONCLUSION: FMT appears to be a potentially useful tool in assisting vitreous surgery including safe ILM peeling.     

HSV-2 alters retinal physiology and morphology bilaterally in mice

Anterior chamber inoculation of 10(4) PFU of the MS strain of HSV-2 resulted in physiologic and morphologic changes in the retina of the inoculated and the uninoculated eyes. In the inoculated eyes, electroretinogram (ERG) depression was first detected on day 3 and abolished ERGs on day 8 postinoculation (PI). The decrease in the ERGs was rapid and the time course was similar for all of the eyes. In spite of a 90% decrease in the amplitude of the b-wave, the retinal sensitivity did not change. Of 23 eyes tested on or after day 10 PI, none had normal, 4.3% had reduced, and 95.6% had abolished ERGs. In the uninoculated eyes, ERG depression was first detected on day 8 and abolished ERGs on day 12 PI. The course of the ERG depression was more variable, and some of the eyes showed a decrease in retinal sensitivity. Of the 22 eyes tested on or after day 17 PI, 18% had normal, 32% had reduced, and 50% had abolished ERGs. The majority (17/33) of the retinas of the inoculated eyes showed panretinal necrosis, although 7 of 33 retinas had pathology confined to the outer layers of the retina. In the uninoculated eyes, only 5 of 30 retinas were necrotic and 14 of 30 retinas had pathology limited to the outer layers of the retina. These observations suggested that the physiologic and morphologic changes progress through two stages: an early stage with reduced ERGs and pathology limited to the outer retinal layers, and a second stage in which the ERG is abolished and the pathologic changes extend into the inner retina. Not all retinas progress to the second stage.     

Retinal function after vitrectomy

PURPOSE: To study retinal function after vitrectomy. METHODS: Core vitrectomy was performed in 12 rabbits under standardized conditions using a vitreous cutting rate of either 600 or 1200 cuts/min. Full-field electroretinography (ERG) and multifocal electroretinography (mfERG) were performed pre- and postoperatively. Morphologic change was monitored by immunohistochemistry directed against glial fibrillary acidic protein (GFAP). RESULTS: Three days postoperatively, the b-wave amplitudes of all cone and rod responses of the ERG were significantly reduced in all vitrectomized eyes. At 28 days, the rod response was still reduced, but returned to normal by 58 days. No correlation was found between vitreous cutting speed and ERG findings. No reduction in the central cone function was detected in the mfERG. GFAP upregulation was found in the entire retina of vitrectomized eyes 3 days after surgery. GFAP expression was present after 28 and 58 days in eyes in which the vitreous cutting rate had been set to 600 cuts/min, but not in the 1200 cuts/min eyes. CONCLUSION: Pars plana vitrectomy transiently affects retinal function in rabbit eyes. Vitreous cutting speed is not related to the reduced function but appears inversely correlated to Müller cell activation, indicating that high-speed vitreous cutters are more lenient to the retina.     

Retinal toxicity of indocyanine green in albino rabbits

PURPOSE: Intravitreal indocyanine green (ICG) is commonly used in vitreoretinal surgery. The purpose of this study was to evaluate possible toxicity of ICG in the retina of albino rabbits. METHODS: Twenty-two albino rabbits were injected intravitreally with 0.1 mL ICG solution in one eye, and three rabbits were studied for the effects of 0.1 mL distilled water. All rabbits were injected intravitreally with 0.1 mL saline into the fellow eye, which served as the control. The electroretinogram (ERG) and visual evoked potential (VEP) were recorded from each rabbit at different time intervals after injection. The rabbits were killed at the termination of the follow-up periods and their retinas prepared for histologic examination at the light microscopic level. RESULTS: Three hours after injection, the ERG responses were reduced in amplitude in all ICG-injected eyes, and the VEPs were of abnormal pattern (reduced amplitude and delayed). Partial dose-dependent recovery was observed during 4 weeks of follow-up. Light microscopy of the retinas of the experimental eyes exhibited considerable damage to all retinal layers in all eyes studied that received the highest ICG dose. CONCLUSIONS: ICG is potentially toxic to all retinal layers of the albino rabbit. Although it is difficult to extrapolate these findings directly to human eyes, caution should be exercised when using ICG intravitreally.