雌激素对光诱导的视网膜电图损害的保护作用

目的:探讨雌激素对光诱导的视网膜电图损害的保护作用。方法:雌性SD大鼠30只,随机分为去势组、去势+雌激素组和正常对照组,每组10只。去势组、去势+雌激素组大鼠接受12h亮12h暗(12∶12)的循环光照射,共14次。行右眼的暗视蓝光ERG、暗视白光ERG检测。结果:正常对照组大鼠暗视蓝光、暗视白光ERGb波振幅分别为87.6±20.2μV、231.2±27.7μV,去势组为24.3±8.4μV、38.5±11.9μV,去势+雌激素组40.0±10.6μV、66.6±17.0μV。去势组与去势+雌激素组之间的差异有显著的统计学差异(q=-3.0129,P=0.005;q=-3.4822,P=0.002)。结论:雌激素对光诱导的视网膜电图损害具有保护作用。     

视网膜中央静脉阻塞对侧眼视网膜电图的观察

本文对31例单眼视网膜中央静脉阻塞（centralretinalveinocclusion，CRVO）患者正常眼底的对侧眼进行了暗视ERGa、b波及OPs各子波峰时值、波幅和OP总合波幅的观察，结果表明，ERG的a、b波及OPs各子波峰时值均延迟，ERGb波波幅异常者占32％，其中b波超高者占29％，b波降低者占3％，OPs主要表现为O2波波幅的降低，异常率42％，异常率随着年龄的增大而增加。在OPs异常的患者中绝大多数存在着血液粘稠度的增高及血脂异常。提示O2波是观察视网膜血液循环障碍的敏感指标。全身因素可以同时影响双眼视网膜功能。     

热休克反应对大鼠视网膜缺血再灌注损伤的防御作用

目的 观察热休克反应对大鼠视网膜缺血再灌注损伤的防御作用。 方法 将20只Wistar大鼠20只眼随机分为4组，每组5只大鼠。行前房灌注（perfusion）平衡盐溶液制造急性高眼压模型,为高眼压组(P组)；在制造急性高眼压模型前24 h向大鼠腹腔内注射槲皮素(quercetin) (400 mg/kg)，为高眼压＋槲皮素组(P+Q组)；在制造急性高眼压模型前24 h 热休克(heat shock)大鼠，为高眼压＋热休克组(P+H组)；分别在制造急性高眼压模型前48 、24 h，向大鼠腹腔内注射槲皮素、热休克大鼠，为高眼压＋槲皮素+热休克组(P+Q+H组) 。按照国际临床视觉电生理学会的标准化方案，采用国特医疗系统对热休克反应后实验性高眼压大鼠模型和HSP70被槲皮素特异性抑制后实验性高眼压大鼠模型进行暗适应视网膜电图(dark adapted electroretinogram, D-ERG)、振荡电位(oscillatory potentials, OPs)和明适应E RG(light adapted ERG, L-ERG)记录。采用Western blotting方法检测各组大鼠视网膜HSP 70表达情况。 结果 P+H组大鼠视网膜HSP70表达在各组大鼠中最高，P+Q、P+Q+H组大鼠视网膜HSP70表达受到抑制。前房灌注后各组大鼠ERG各波潜伏期延长、幅值减小，P+H组D-ERG的b波、OPs的O₂波的幅值较P组高。灌注0 h后，P+H组各波幅值显著增高(P值均<0.05)；灌注24 h 后，P+H组大鼠视网膜功能恢复较P组好。P+Q、P+Q+H组大鼠灌注后ERG各波及OPs的O₂波潜伏期最长，幅值最低，甚至消失。 结论 热休克反应可以提高大鼠视网膜细胞对缺血再灌注损伤的防御作用。 （中华眼底病杂志，2003，19：117-120）     

高血糖对实验性糖尿病大鼠视网膜电图的影响

目的观察糖尿病大鼠ERG和OPs的变化情况,探讨糖尿病对大鼠FERG和OPs的影响。方法将100只大鼠分为正常组10只和糖尿病组90只。糖尿病组用STZ造模,6个月后将符合条件的大鼠纳入观察组。检测6、9个月时大鼠ERG和OPs的表现。结果糖尿病大鼠视网膜电图a波、b波、OPs振幅有下降趋势,峰潜时延长,与对照组大鼠相比有差异(P<0.01);9个月时糖尿病大鼠a波、b波、OPs振幅降低,峰潜时延迟,与6个月时比较有显著差异(P<0.01或0.05)。结论高血糖可使糖尿病大鼠ERG和OPs振幅下降,峰潜时延长;且随病程的延长其影响逐渐增强。     

视网膜电图和多焦视网膜电图ON/OFF反应的研究进展

ON/OFF反应是人们从视网膜电生理反应中记录到的视网膜给光、撤光反应。它是通过不同的光感受器细胞形成不同的ON/OFF通路来完成。视网膜电图（ERG）和多焦视网膜电图（mf-ERG）ON/OFF反应的异常可明确提示ON/OFF通路及通路相关细胞的异常,在临床多种疾病,如先天性静止性夜盲,X连锁青年性视网膜病变等的诊断与治疗中有着重要意义。就ON/OFF通路（视锥ON/OFF通路,视杆ON/OFF通路,视杆慢快ON/OFF通路）和ERG、mfERGON/OFF反应的最佳记录方法、条件及在临床中的应用进行综述。     

视网膜电图对视网膜血管阻塞的功能评估

目的：用视网膜电图评估视网膜血管阻塞的功能改变。方法：３０例视网膜中央静脉阻塞,１５例视网膜分支静脉阻塞,７例视网膜中央动脉阻塞和６例视网膜分支动脉阻塞按照ＩＳＣＥＶ的ＥＲＧ标准进行全视野网膜电图的检测。用Ｉ１蓝光、Ｉ１６红光和Ｉ１６白光估计暗视ＥＲＧ,用Ｉ１６红光和Ｉ８白光估计明视ＥＲＧ。记录ａ波和ｂ波的振幅和潜伏期及震荡电位。结果：视网膜血管阻塞的震荡电位异常率最高,其次为ｂ波;ＥＲＧ的异常率     

大鼠玻璃体内注射二甲基亚砜对视网膜电图的影响

目的探讨不同浓度二甲基亚砜（dimethyl sulfoxide，DMSO）对大鼠视网膜电图（electroretinogram，ERG）的影响。方法24只SD大鼠随机分为4组，将不同浓度的DMSO溶液分别注入各组大鼠实验眼的玻璃体腔，经玻璃体液稀释后，DMSO在玻璃体腔的终浓度依次为0.1％、0.2％、0.5％和1．0％。对侧眼作为对照注入等量生理盐水。分别在注射前及注射后第2、第4、第7、第10天对暗适应ERGb波进行检查。结果注射DMSO溶液后，0.5％、1．0％组实验眼b波幅值较对照眼显著上升，而在0.2％、0.1％组却无显著性差别。注射后，各组实验眼b波潜时与对照眼相比差异均无显著性。结论DMSO在玻璃体腔的终浓度≥0．5％时会影响视网膜的功能，而浓度≤0.2％时则无明显影响，因此在动物实验中不能忽视DMSO的浓度因素对视网膜功能的影响。     

Math5对视网膜神经节细胞的分化调控

视网膜神经节细胞是视网膜发育中第一个产生的神经元,它的分化由视网膜前体细胞的内部信号和视网膜微环境的外部信号共同决定。Math5是Ath5在小鼠的表达形式,后者是视网膜神经节细胞分化的必要基因,但视网膜神经节细胞的分化还需要其他基因共同参与。本文就Math5 对视网膜神经节细胞的分化调控及其与其他基因的相互作用作一综述。     

早期糖尿病视网膜病变的视网膜电图研究

目的：研究早期糖尿病视网膜病变（diabeticretinopathy,DR) 的视网膜电图震荡电位（Oscillatory potentials,OPs)和图形视网膜电图（Pettern electroretinogram,P-ERG)的变化特点,借以早期诊断DR。方法：对20例（40眼）正常和50例（113眼）糖尿病病人进行OPs和P－ERG检测。结果：当糖尿病病人眼底尚未出现改变时,P－ERG的b波波幅和OPs各子波波幅及总波幅已降低。随着DR的发展,各参数的异常率逐渐上升,各波波幅也随之下降,潜伏期延长。OPs的O3波波幅和总波幅以及P－ERG的b波波幅较其它指标具有较高的敏感性,其中O3波波幅为最敏感的指标。结论：OPs的O3波波幅和总波幅等参数能够作为视觉电生理的功能性指标预测DR的发生,在DR的早期诊断和评价DM的疗效方面有临床应用价值。     

视网膜脱离的视网膜电图分析

目的　分析视网膜脱离的视网膜电图的改变。方法　对 5 0例视网膜脱离患者的视网膜电图检查分析其变化。结果　与正常人相比 ,视网膜脱离的 a,b振幅降低 ,潜时延长。结论　视网膜电图对视网膜脱离患者的视网膜功能提供了一个无损伤的途径 ,对判定病情及预后有一定的指导意义。     

ZX-5及其光学异构体对兔眼血流和大鼠视网膜功能恢复的影响

目的:研究ZX-5对缺血后视网膜功能的恢复作用,并比较其光学异构体(R,R)-ZX-5和(S,S)-ZX-5对脉络膜血流及缺血后视网膜功能恢复的影响。方法:用彩色微球技术研究兔高眼压下(40mmHg)脉络膜血流的变化。用视网膜电生理仪测量b波,评价大鼠缺血后视网膜功能的恢复情况。结果:10g/L(R,R)-ZX-5滴眼液50μL能在不同时间点提高脉络膜血流(P<0.05),而(S,S)-ZX-5在相同条件下对提高脉络膜血流没有影响。ZX-5和(R,R)-ZX-5在不同时间点对视网膜缺血后功能恢复作用明显(P<0.05),(R,R)-ZX-5的作用优于ZX-5;而(S,S)-ZX-5对缺血后视网膜功能的恢复作用不明显。结论:ZX-5和(R,R)-ZX-5对增加脉络膜血流量和促进视网膜功能的恢复有显著功效,(R,R)-ZX-5恢复视网膜功能的作用更强,有可能进一步开发成有效防治眼血流障碍相关性眼病的药物。     

Effects of ZX-5 and its optical isomers on ocular blood flow in rabbits and retinal function recovery in rats

AIM: The effects of ZX-5, as nitric oxide (NO) donor, on ocular blood flow has been investigated using colored microsphere technique in previous study. The relationship between the production of NO by ZX-5 and ocular blood flow has been evaluated. ZX-5 has been shown to have strong positive effect on increasing choroidal blood flow. However, the effect of ZX-5 on retinal function recovery, the effects of its optical isomers, (R, R)-ZX-5 and (S, S)-ZX-5, on choroidal blood flow and retinal function recovery have not been studied and merit investigation. · METHODS: Colored microsphere technique was used for in vivo experiments to determine choroidal blood flow of ocular hypertension (40mmHg) in rabbit eyes. Electroretinography was used to measure the b-wave recovery as an indication of retinal function recovery. · RESULTS: (R, R)-ZX-5 increased choroidal blood flow at 10g/L, 50μL instillation into eyes at all time points (P <0.05). (S, S)-ZX-5 was not effective in increasing choroidal blood flow. ZX-5 and (R, R)-ZX-5 showed significant effects in retinal function recovery after ischemia of the retina at all time points (P <0.05); whereas (S, S)-ZX-5 did not show significant effect on recovery of b-wave after ischemia at most time points except at 120 and 240 minutes. · CONCLUSION: ZX-5 and (R, R)-ZX-5 have high potency in increasing the choroidal blood flow and improving the retinal function recovery. It is hoped that they could be used for the prevention/treatment of ocular blood flow related eye diseases.     

Clinicopathologic analysis of 166 patients with primary acquired nasolacrimal duct obstruction.

OBJECTIVE: To determine the prevalence of lacrimal sac pathology in patients undergoing dacryocystorhinostomy (DCR) for primary acquired nasolacrimal duct obstruction (PANDO). DESIGN: Observational case series. PARTICIPANTS: One hundred sixty-six patients with symptoms of PANDO. METHODS: A total of 202 lacrimal sac biopsies were obtained from 166 patients undergoing external DCR procedures for symptoms of PANDO. MAIN OUTCOME MEASURES: Patient demographics, presenting symptoms and signs, relevant history, and assessment of the nasolacrimal system were recorded. All lacrimal biopsy specimens were examined histopathologically. RESULTS: A total of 118 patients (71%) were female and 48 patients (29%) were male. The mean age was 60.7 years (range, 21-93 years). All patients demonstrated epiphora, and 32 patients had dacryocystitis. Duration of symptoms ranged from 6 weeks to 50 years. No lacrimal sac tumors were detected. Sixty-five percent of specimens demonstrated chronic inflammation. CONCLUSIONS: No neoplasms were detected among 202 lacrimal sac specimens from 166 patients with symptoms of PANDO. Most lacrimal sac specimens demonstrated chronic inflammatory changes. We conclude that a lacrimal sac biopsy should be performed when there is suspicion of a neoplasm based on the clinical, historical, or intraoperative findings, rather than routine biopsy of all patients with PANDO.     

Composition and synthesis in vivo of water-soluble proteins in the rat ocular lens: normal and cataractous

This study describes the composition and synthesis in vivo of the water-insoluble proteins in normal and cataractous rat ocular lens. Cataracts of the lens nucleus were induced by treatment of the young rat with U18666A, 3β-(2-diethylaminoethoxy)androst-5-en-17-one. HCl. Opaque lens contained more insoluble proteins and incorporated more intraocularly injected [³H]leucine into these proteins than clear lens. Insoluble proteins from both clear and opaque lens consisted of classes in three mol. wt. ranges; > 68 000, 35 000–60 000 and 16 000–22 000. Treatment with mercaptoethanol produced changes in the electrophoretic profiles of the 35 000–60 000 and 16 000–22 000 mol. wt. classes of proteins from both normal and opaque lens; however, the higher mol. wt. class from only the opaque lens was reduced to smaller components. The lowest mol. wt. class accounted for over 50% of the total water-insoluble protein in both types of lens. [³H]leucine was incorporated into the protein classes roughly proportionate to their relative concentrations, although there was a tendency for normal lens to incorporate more label into peak 1 and 2 proteins and for cataractous lens to incorporate more into peak 3 proteins. In general, however, the greater concentration of water-insoluble protein in this cataract appeared due to a proportionately increased formation of the same proteins present in normal lens. In contrast to human senile cataracts, the opaque rat lens did not preferentially accumulate disulfidelinked very high mol. wt. insoluble protein. However, the aged (i.e. pre-existing) higher mol. wt. insoluble proteins of the U18666A cataract appeared different from those newly synthesized, since the aged proteins were reduced under conditions not affecting those newly synthesized.     

Risk of obstructive sleep apnea in open-angle glaucoma versus controls using the STOP-Bang questionnaire

Objective

To compare the percentage of patients at risk for obstructive sleep apnea (OSA) in open-angle glaucoma (OAG) versus controls using the STOP-Bang questionnaire.

Fixation parameter test-retest repeatability of the worse eye in central field loss

Objective

Patients with bilateral central field loss develop peripheral retinal loci (PRLs) in the functional eccentric retina. PRL characteristics and visual performance in the better-seeing eye (BE) of these patients have previously been reported. In this study, we determined the test-retest repeatability of fixation parameters, including fixation stability, PRL eccentricity, and PRL span in the worse-seeing eye (WE).

Glutamate receptors and circuits in the vertebrate retina

We survey the evidence for L-glutamate's role as the primary excitatory neurotransmitter of vertebrate retinas. The physiological and molecular properties of glutamate receptors in the retina are reviewed in relation to what has been learned from studies of glutamate function in other brain areas and in expression systems. We have focused on (a) the evidence for the presence of L-glutamate in retinal neurons, (b) the processes by which glutamate is released, (c) the presence and function of ionotropic receptors for L-glutamate in retinal neurons, (d) the presence and function of metabotropic receptors for L-glutamate in retinal neurons, and (e) the variety and distribution of glutamate transporters in the vertebrate retina. Modulatory pathways which influence glutamate release and the behavior of its receptors are described. Emphasis has been placed on the cellular mechanisms of glutamate-mediated neurotransmission in relation to the encoding of visual information by retinal circuits.     

Amino acid neurochemistry of the vertebrate retina

The dominant neurochemicals involved in encoding sensory information are the amino acid neurotransmitters, glutamate, γ-aminobutyrate (GABA) and glycine which mediate fast point-to-point synaptic transmission in the retina and other parts of the central nervous system. The relative abundance of these neurochemicals and the existence of neuronal and glial uptake mechanisms as well as a plethora of receptors support the key role these neurochemicals play in shaping neural information. However, in addition to subserving neurotransmitter roles, amino acids subserve normal metabolic/cellular functions, may be precursors for other amino acids, and may also be associated with protein synthesis. Post-embedding immunocytochemistry of small molecules has allowed the characterization of multiple amino acid profiles within subpopulations of neurons in the vertebrate retina. The general theme emerging from these studies is that the retinal through pathway uses glutamate as its neurotransmitter, and the lateral elements, GABA and/or glycine. Co-localization studies using quantitative immunocytochemistry have shown that virtually all neuronal space can be accounted for by the three dominant amino acids. In addition, co-localization studies have demonstrated that there are no purely aspartate, glutamine, alanine, leucine or ornithine immunoreactive neurons and thus these amino acids are likely to act as metabolites and may sustain glutamate production through a multitude of enzymatic pathways. The mapping of multiple cellular metabolic profiles during development or in degenerating retinas has shown that amino acid neurochemistry is a sensitive marker for metabolic activity. In the degenerating retina, (RCS retina), neurochemical anomalies were evident early in development (from birth), even before photoreceptors mature at PND6-8 implying a generalized metabolic dysfunction. Identification of metabolic anomalies within subpopulation of neurons is now possible and can be used to investigate a multitude of retinal functions including amino acid metabolic and neurochemical changes secondary to external insult as well as to expand our understanding of the intricate interrelationship between neurons and glia.     

Cellular responses following retinal injuries and therapeutic approaches for neurodegenerative diseases

Retinal neurodegenerative diseases like age-related macular degeneration, glaucoma, diabetic retinopathy and retinitis pigmentosa each have a different etiology and pathogenesis. However, at the cellular and molecular level, the response to retinal injury is similar in all of them, and results in morphological and functional impairment of retinal cells. This retinal degeneration may be triggered by gene defects, increased intraocular pressure, high levels of blood glucose, other types of stress or aging, but they all frequently induce a set of cell signals that lead to well-established and similar morphological and functional changes, including controlled cell death and retinal remodeling. Interestingly, an inflammatory response, oxidative stress and activation of apoptotic pathways are common features in all these diseases. Furthermore, it is important to note the relevant role of glial cells, including astrocytes, Müller cells and microglia, because their response to injury is decisive for maintaining the health of the retina or its degeneration. Several therapeutic approaches have been developed to preserve retinal function or restore eyesight in pathological conditions. In this context, neuroprotective compounds, gene therapy, cell transplantation or artificial devices should be applied at the appropriate stage of retinal degeneration to obtain successful results. This review provides an overview of the common and distinctive features of retinal neurodegenerative diseases, including the molecular, anatomical and functional changes caused by the cellular response to damage, in order to establish appropriate treatments for these pathologies.