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PubMed2002

Vitamin E deficiency in dogs with retinal pigment epithelial dystrophy.

The role of vitamin E deficiency in the development of retinal pigment epithelial dystrophy was investigated in 11 cocker spaniels and four other dogs. The concentration of alpha-tocopherol was measured by high performance liquid chromatography in plasma samples obtained from the affected dogs and from 28 ophthalmoscopically normal, healthy control dogs. The mean (sd) plasma alpha-tocopherol concentration in the normal dogs was 20.2 (7.1) microg/ml, compared with 1.14 (0.67) microg/ml in the 11 affected cocker spaniels. The difference between the two groups remained highly significant when the alpha-tocopherol concentrations were expressed relative to the concentrations of the plasma lipids cholesterol and triglycerides. Low plasma concentrations of alpha-tocopherol were observed in the four affected dogs of other breeds, but the finding was not so consistent. The plasma lipid concentrations were normal in the affected dogs. The deficiency of alpha-tocopherol in the affected dogs appeared to be primary, because there was no clinical, biochemical or pathological evidence of underlying disease, or any indication of a dietary deficiency which might have contributed to the low concentrations of alpha-tocopherol.

Animals↗
PubMed2003

VEGF-TRAP(R1R2) suppresses choroidal neovascularization and VEGF-induced breakdown of the blood-retinal barrier.

Vascular endothelial growth factor (VEGF) plays a central role in the development of retinal neovascularization and diabetic macular edema. There is also evidence suggesting that VEGF is an important stimulator for choroidal neovascularization. In this study, we investigated the effect of a specific inhibitor of VEGF, VEGF-TRAP(R1R2), in models for these disease processes. VEGF-TRAP(R1R2) is a fusion protein, which combines ligand binding elements taken from the extracellular domains of VEGF receptors 1 and 2 fused to the Fc portion of IgG1. Subcutaneous injections or a single intravitreous injection of VEGF-TRAP(R1R2) strongly suppressed choroidal neovascularization in mice with laser-induced rupture of Bruch's membrane. Subcutaneous injection of VEGF-TRAP(R1R2) also significantly inhibited subretinal neovascularization in transgenic mice that express VEGF in photoreceptors. In two models of VEGF-induced breakdown of the blood-retinal barrier (BRB), one in which recombinant VEGF is injected into the vitreous cavity and one in which VEGF expression is induced in the retina in transgenic mice, VEGF-TRAP(R1R2) significantly reduced breakdown of the BRB. These data confirm that VEGF is a critical stimulus for the development of choroidal neovascularization and indicate that VEGF-TRAP(R1R2) may provide a new agent for consideration for treatment of patients with choroidal neovascularization and diabetic macular edema.

Animals↗
PubMed2003

Transscleral thermotherapy: short- and long-term effects of transscleral conductive heating in rabbit eyes.

OBJECTIVE: To determine the highest safe treatment temperature, at 30- and 60-second exposure durations, for transscleral thermotherapy (TSTT) of choroidal melanoma. METHODS AND DESIGN: Transscleral conductive heating was performed in 15 rabbits at 50 degrees C to 70 degrees C for 30 or 60 seconds. The thermal lesions in the ocular fundus were monitored for 4 months with ophthalmoscopic, photographic, and fluorescein angiographic examination. Histologic examination included polarized light microscopy. RESULTS: The effect of TSTT was similar for both exposure durations. Vascular occlusion in the retina and choroid developed at temperatures of 55 degrees C and higher. After heating at 60 degrees C, scleral collagen fibers developed a minimal undulation; at 65 degrees C, they became clearly undulated. The undulation resolved in the 3 to 4 months after heating. Heating at 70 degrees C caused persistent severe damage to the sclera. Retinal tears developed after heating at 65 degrees C and 70 degrees C. CONCLUSIONS: A temperature of 65 degrees C was found to be the highest temperature that did not cause permanent damage to the sclera at both exposure durations. A temperature of 60 degrees C may be the optimal temperature for TSTT of choroidal melanoma because retinal tears may develop at 65 degrees C. CLINICAL RELEVANCE: In TSTT, the temperature levels reached are cytotoxic for choroidal melanoma as well as intrascleral tumor cells. Occlusion of choroidal vessels induced by TSTT may contribute to tumor necrosis because these vessels serve as feeder vessels for the tumor.

Animals↗
PubMed1999

Development of laser-induced retinal damage in the rabbit.

BACKGROUND: Laser lesions may induce retinal damage that is larger than expected from the size of the coagulated area. This study was designed to follow the development of laser-induced reduction in retinal function and to correlate it with structural changes. METHODS: Pigmented rabbits were treated in one eye with 225 argon laser lesions. The ERG responses were recorded at different times after treatment. The effect of the laser treatment upon the functional integrity of the retina was assessed from the ERG responses. Structural damage was examined by light microscopy. RESULTS: Shortly (1-2 h) after laser treatment, the ERG responses were reduced by about 50%. ERG deficit continued to develop and reached a maximal level about 24 h after treatment. Thereafter, slow recovery was observed but permanent deficit, relative to the initial laser effect, was seen even 30 days after treatment. Histological observations indicated extensive serous retinal detachment between laser lesions that developed within 24 h after treatment. At 30 days post-treatment, lesioned areas were completely destroyed and heavily pigmented. The retina between lesions was attached to the pigment epithelium but exhibited different degrees of structural damage. CONCLUSIONS: The immediate laser damage is confined to the coagulated areas while secondary functional damage develops within 24 h and probably reflects serous retinal detachment between lesions. The serous retinal detachment completely resolves with time but may induce permanent structural abnormalities in non-coagulated retinal areas that is reflected in a functional deficit larger than the initial laser effect.

Animals↗
PubMed1997

Transient expression of PG-M/versican, a large chondroitin sulfate proteoglycan in developing chicken retina.

We previously showed the expression of PG-M/versican in embryonic chicken retina. In this study, we characterized the alternatively spliced forms of PG-M/versican and their developmental regulation to investigate the implication of PG-M/versican in neurite outgrowth from retinal cells during development. On day 5, the immunolocalization of PG-M was first observed at the inner surface of neural retina. On day 7, the pronounced staining was observed in the nerve fiber layer and inner plexiform layer where neural networks of ganglion cells were being formed. As the development proceeded, more intensive staining was observed in these layers. The staining peaked on day 14 and then decreased. Northern analysis and western blotting revealed the presence of a single-sized transcript (13 kb) and the PG-M/versican core protein (550 kDa) on day 14, but the absence of any transcripts or protein bands on day 20, indicating a transient expression of PG-M+ (VO), the alternatively spliced form with the most abundant sites for the chondroitin sulfate attachment. Taken together, it is likely that PG-M/versican is involved in neurite outgrowth from ganglion cells during retinal development, and antiadhesion activity of its chondroitin sulfate chains may be important for regulation.

Alternative Splicing↗
PubMed1980

[Retinal detachment limited by spontaneously developing pigment bands (author's transl)].

A report on twelve patients seen during a period of ten years, all of whom presented with retinal detachment limited by spontaneously developing "barriers" consisting of heavily pigmented or depigmented bands. The strength of these bands is discussed. On the basis of clinical experience they can only be considered stable in rare cases; the detachment usually progresses beyond them in time.

Adolescent↗
PubMed1995

Accumulation of 3H-phosphoinositides mediated by muscarinic receptors in the developing chick retina: inhibition of carbachol-induced response by glutamate receptors.

In the present work we show the development of carbachol-induced accumulation of 3H-inositol phosphates (3H-InsPs) in the chick embryonic retina and its regulation by glutamate receptors. Although basal levels of 3H-InsPs increased during development, the retinal response to carbachol was high in the early developing stages and decreased after synaptogenesis in the retina. Eserine also stimulated the turnover of phosphoinositides in the embryonic but not in the mature retina. The effect of eserine could be blocked by atropine, suggesting that acetylcholine could be released from developing retina cells and further stimulate the turnover of InsPs in the embryonic tissue. Our data also show that muscarinic stimulation of turnover of 3H-InsPs could be blocked by stimulation of glutamatergic ionotropic receptors. Moreover, the effect of glutamate agonists did not seem to be mediated by the release of other neurotransmitters such as GABA, glycine, adenosine, or dopamine from the tissue because these neurotransmitters did not interfere with the retinal response to carbachol. These results suggest that muscarinic activation of phosphoinositide turnover occurs mainly in the embryonic retina and that activation of glutamate receptors can inhibit directly the muscarinic stimulation of hydrolysis of 3H-InsPs in this tissue.

Animals↗
PubMed2006

Radial optic neurotomy for central retinal vein occlusion: 117 consecutive cases.

PURPOSE: Venous occlusive disease is the second leading cause of permanent retinal vascular blindness. The anatomy of the optic disk including the cribriform plate and scleral ring may contribute to the development of retinal vasoocclusive diseases. Neurovascular compression within the confined space at this location (scleral outlet) may play a pathoetiologic role in central retinal vein occlusion (CRVO). We developed a surgical procedure (radial optic neurotomy [RON]) to open this space and relieve pressure on the central retinal vein. METHODS: Pars plana vitrectomy with RON was performed on 117 consecutive patients with CRVO and severe loss of vision (defined as 20/200 or worse). Patients were observed with serial fundus photography, fluorescein angiography, determination of Snellen visual acuity, and biomicroscopy for anterior segment neovascularization. RESULTS: There were no serious complications noted with this procedure. Anatomical and clinical improvement as determined by fundus examination, fundus photography, and fluorescein angiography was found in 95% of patients. Snellen visual acuity improved by an average of 2.5 lines (range, 1-12 lines) in 71% of patients. Two or more lines were gained in 53% of patients, and > or = 4 lines were gained in 25%. Anterior segment neovascularization was found in 6% of patients with CRVO. CONCLUSIONS: Surgical decompression of CRVO via RON is a technically feasible and safe procedure that was associated with anatomical resolution of CRVO in 95% patients and improved visual function in 71%.

Adult↗
PubMed2002

Rate of resolution of exudative retinal detachment after plaque radiotherapy for uveal melanoma.

OBJECTIVES: To determine the clinical relevance of exudative retinal detachment (ERD) and the rate of ERD resolution after plaque radiotherapy of posterior uveal melanomas. METHODS: Retrospective, nonrandomized study of 135 consecutive patients with posterior uveal melanoma treated by iodine 125 plaque radiotherapy. Extent of ERD and tumor thickness were assessed before radiotherapy and at postoperative follow-up visits. Local tumor control was assessed at each follow-up visit. RESULTS: An ERD was present in 71 patients (53%) and was a risk factor for local treatment failure (P =.03). The ERD resolved after radiotherapy in 59 (83%) of the 71 patients. The ERD resolved within 1 year in 64 patients (90%) (mean time to resolution, 5.6 months). The rate of ERD resolution correlated with the rate of decrease in tumor thickness (P =.004). The ERD did not resolve and the tumor thickness continued to increase in 5 patients, who required further intervention. A recurrent retinal detachment developed in 5 patients, who were diagnosed as having rhegmatogenous retinal detachment (3 patients) and lipid exudation secondary to tumor vasculopathy (2 patients). Two patients with local tumor recurrence did not develop a recurrent ERD. Local tumor control was achieved in 130 patients (96%). CONCLUSIONS: An ERD may be a risk factor for local failure after plaque radiotherapy for uveal melanoma. If an ERD does not resolve within 9 to 12 months of radiotherapy and the tumor is not regressing, treatment failure should be suspected. A recurrent ERD does not necessarily represent local tumor recurrence.

Adult↗
PubMed1992

T cell depletion increases susceptibility to murine cytomegalovirus retinitis.

To study the effect of immunosuppression on the development of murine cytomegalovirus (MCMV) retinitis, BALB/c mice were immunosuppressed with methylprednisolone (a corticosteroid) and/or with antibodies against CD4+ and CD8+ T cells and inoculated with low-dose MCMV (5 x 10(2) plaque-forming units) by the supraciliary route. Nonimmunosuppressed mice inoculated with low-dose MCMV by the supraciliary route did not develop necrotizing retinitis. By contrast, 78-100% of immunosuppressed mice developed retinitis after inoculation of low-dose MCMV. To study the effect of depletion of individual T cell subsets, mice were depleted of either CD4+ or CD8+ T cells and inoculated with low-dose MCMV by the supraciliary route. The frequency of retinitis in CD4-depleted mice (30%) was not significantly different from that of nonimmunosuppressed control mice (0%). The frequency of retinitis in the CD8-depleted group (80%) was similar to that observed in mice immunosuppressed with corticosteroid alone (90.9%), with antibodies to both T cell subsets (100%), or with steroid and both T cell subset antibodies (100%). These results support the conclusion that the CD8+ T cell subset is responsible for control of ocular MCMV infection. Furthermore, these results suggest that the CD8+ T cell subset may be important in preventing ocular CMV infection in immunosuppressed patients.

Animals↗
PubMed2006

Neurensin-1 expression in the mouse retina during postnatal development and in the cultured retinal neurons.

Neurensin-1/Neuro-p24 (previously named Neuro-p24) is a neuron-specific membrane protein that is localized particularly in neurites. Neurensin-1 is considered to play an essential role in neurite extension during nervous development, regeneration and plasticity. To understand what role Neurensin-1 plays in retinal differentiation, we examined Neurensin-1 distribution and gene expression pattern in the postnatally developing retina of the mouse, because the retina is an excellent model for nervous development. In the postnatal day (PD) 1 retina, intense Neurensin-1 immunoreactivity was found in the optic nerve fiber layer. Faint staining was seen in the ganglion cells, presumptive amacrine and horizontal cells. As the postnatal development proceeded, the optic fibers became more intensely stained in addition to other parts of the retina such as the ganglion cells, inner plexiform layer and horizontal cells. In PD 10 retinas, the horizontal cell processes showed a prominently stained configuration. As the retina developed further to attain maturity, the staining in the retina became less pronounced, although the optic nerves remained positively stained. The distribution of Neurensin-1 mRNA was consistent with these results and confirmed that the ganglion, amacrine and horizontal cells actively synthesize Neurensin-1 in the developing retina. In the retinal cell culture from newborn mice, two types of neural cells were stained for Neurensin-1, one of which showed long processes and appeared presumptive ganglion cells. These results suggest that Neurensin-1 plays a role in the fiber extension of the retinal neurons, as has been observed in other central nervous tissues, and indicate that the developing retina is a suitable experimental model for the analysis of Neurensin function, both in vivo and in vitro.

Animals↗
PubMed1996

Evidence that retinal ganglion cell density affects foveal development.

The monkey's foveola normally contains significant numbers of retinal ganglion cells. The somata of foveola cells are larger than those of other cells in the central retina. Their dendritic fields are up to 50 times larger in area than those of nearby cells in the foveal slope. Experimentally induced reductions in the number of ganglion cells in central retina results in alterations in the size and distribution of cells within the foveola. In these animals the foveola is abnormally small and contains an abnormally large number of cells having smaller than normal cell bodies and dendritic fields. These studies indicate that the formation of the foveola as well as the development of the morphology of cells within the foveola and foveal slope depend during development on high densities of retinal ganglion cells within the central retina.

Animals↗
PubMed1998

[Ocular fundus lesions in systemic lupus erythematosus model mice].

To evaluate spontaneous development of the ocular fundus abnormalities associated with collagen disease, we investigated the ocular fundus lesions in systemic lupus erythematosus (SLE) models. (NZW x BXSB) F1 mice were employed as SLE models with antiphospholipid syndrome. The abnormal findings in the ocular fundus were recorded with a fundus camera for small animals (KOWA Co., Ltd.), and the chorioretinal lesions were studied histopathologically. As in the systemic symptoms of SLE, the incidence of ocular fundus abnormalities in these (NZW x BXSB) F1 mice was significantly higher in males than in females, suggesting the influence of the Yaa (Y chromosome-linked autoimmune acceleration) gene. Lesions in the fundus appeared in the form of white spots, which increased in number along with the course of the disease. The lesion developed into retinal detachment in some animals. Dilatation of veins and narrowing of arteries were marked. These lesions were very similar to multifocal posterior pigment epitheliopathy (MPPE) in humans in that white spots appear first and then develop into exudative retinal detachment caused by retinal pigment epithelial disorder. Histopathological findings included 1. structural destruction of the photoreceptor cell layer, 2. degeneration and loss of the retinal pigment epithelium, and 3. narrowing and occlusion of the choriocapillaris associated with thrombus formation, cellular infiltration into the surrounding tissues, and wall thickening of the choroidal arterioles. The study of these SLE mouse may contribute to the elucidation of abnormalities in the fundus associated with collagen diseases, including the relationship between thrombus formation and antiphospholipid syndrome.

Animals↗
PubMed1988

Development of cell density gradients in the retinal ganglion cell layer of marsupials.

An area centralis and visual streak, specializations of high cell density in the mammalian retinal ganglion cell layer, develop from a more uniform cell distribution. In the wallaby and kangaroo, this transition is first seen 60 days postnatally. Total live cell numbers in this layer fall by approximately one-third as these specializations start to appear and dying cells are seen. However, dying cells have already become concentrated at the retinal rim prior to the emergence of live cell density gradients. Our results suggest that cell death may partially sculpt patterns of live cells, particularly by lowering densities around the entire far periphery. Studies of cell division demonstrate that ganglion cells are generated and enter the ganglion cell layer before the area centralis and visual streak are formed. However, cell addition to the inner and outer nuclear layers continues as cell density gradients become apparent in the ganglion cell layer. Furthermore, this late cell generation ceases first in areas adjacent to the presumptive area centralis. The differential distribution of such prolonged cell addition to the inner and outer nuclear layers may result in an asymmetric expansion of the retina. This process would partially explain the changing topography of cells in the ganglion cell layer. Mathematical analysis of patterns of overall retinal growth support this interpretation.

Animals↗
PubMed1985

Retinal pigment epithelial correlates of avian retinal degeneration: electron microscopic analysis.

The delayed amelanotic (DAM) strain of domestic chicken is characterized by an early, developmental onset of choroidal inflammation and destruction of both feather and choroidal melanocytes. Secondarily, retinal pigment epithelial (RPE) cells in the peripapillary region develop abnormalities, and a series of progressive histopathological changes ensues which includes reduction and ultimate loss of RPE-melanin granules and RPE-cell atrophy. The earliest sign of RPE-cell abnormality is a dramatic alteration in the distribution of intracellular melanin granules. Apical processes also show a lessening of contact with photoreceptor outer segments, leading in more advanced stages to their retraction and development of retinal detachments. Other progressive alterations in RPE cells include disorganization and loss of basal infoldings; size reductions and density increases in both mitochondria and myeloid bodies from early to advanced stages; appearance of large macrophages in the subretinal space; Loss of intercellular junctional complexes; and progressive reduction in the density of melanin granules. These abnormalities appear to spread in a cell-by-cell, radial pattern, until widespread areas of the retina become severely pathologic and atrophic. The DAM chorioretinal disorder appears to show many of the histopathologic features which characterize experimentally induced uveitis and other ocular diseases which may result from hypersensitivity to, or autoimmune reaction against, pigments of the uveal tract.

Animals↗
PubMed1982

Clinical and experimental studies on retinal neovascularization. XXXIX Edward Jackson Memorial Lecture.

Retinal neovascularization is a serious complication of the retinopathy associated with diabetes, branch vein occlusion, sickle cell anemia, and retrolental fibroplasia. Retinal capillary nonperfusion, demonstrated on fluorescein angiography, precedes the development of neovascularization in each of these conditions. Our working hypothesis is that the nonperfused (ischemic or hypoxic) retina liberates a vasoproliferative or angiogenic substance. Although I have delineated the clinical and experimental observations relating to the hypothesis of an ischemic-mediated angiogenesis substance, other postulated mechanisms for the development of retinal neovascularization may be involved. Recent observations on the experimental model of retrolental fibroplasia have demonstrated the markedly abnormal persistence and apparent proliferation of the hyaloid vessels in mice following oxygen-induced retinal vascular closure.

Animals↗
PubMed1983

Experimental retinal autoimmunity (ERA) in strain 13 guinea pigs: induction of ERA-retinopathy with rhodopsin.

Strain 13 guinea pigs injected with either homologous or bovine rhodopsin, the visual pigment of the retinal outer segments, in complete Freund's adjuvant (CFA) developed experimental retinal autoimmunity (ERA). Initial clinical signs of disease were seen within 21 days after immunization. Pathologic examination of the eyes revealed the presence of inflammatory cells in the choroid and the destruction of the retinal rod outer segments. The unique feature of this disease is that despite the destruction of the inner and outer segments of the retina, at no time is there a substantial inflammatory cell infiltrate. Even as late as 45 days after immunization, when destruction of the retinal ganglion cell layer was noted, no inflammatory cells were detected in the retina. These findings suggest that the retinal inner and outer segments are the target of the autoimmune reaction subsequent to sensitization with purified rhodopsin-CFA.

Animals↗
PubMed1995

A prospective study of dense spontaneous vitreous hemorrhage.

PURPOSE: We studied the incidence of vitreous hemorrhage in a well-defined population to determine the underlying causes of such hemorrhages. METHODS: We prospectively studied all eyes with dense spontaneous first-time vitreous hemorrhage during a 2 1/2-year period in the greater Göteborg area (542,000 inhabitants). Follow-up time was one year. RESULTS: Ninety-four patients (95 eyes) were included, corresponding to a yearly incidence of seven cases per 100,000 inhabitants. Because of demographic factors and the organization of Swedish ophthalmologic care, we believe that this is close to the true incidence. The cause of vitreous hemorrhage could be verified in all but four eyes but frequently not until late in the follow-up period. The most common underlying cause was vitreous detachment and traction to a retinal vessel (39 eyes). In 28 of these eyes a retinal tear was also present. Five of these eyes developed a retinal detachment. In 19 eyes, bleeding was caused by proliferative diabetic retinopathy. This figure was relatively smaller than in previous studies. Retinal vein occlusion was the cause of hemorrhage in 15 eyes. Retinal macroaneurysm (seven eyes) was an easily overlooked cause, often diagnosed late in the follow-up period. CONCLUSIONS: Because of the common diagnostic difficulties and the frequent need for laser treatment, vitrectomy, or both, it is recommended that eyes with vitreous hemorrhage be followed up in centers with ultrasonographic and surgical expertise.

Adult↗