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At least 721 records · Page 40Linked to original sources
PubMed1994

Immunohistochemical localization of blood-retinal barrier breakdown sites associated with post-surgical macular oedema.

Post-surgical macular oedema results from blood-retinal barrier breakdown, but it is not accompanied by structural abnormalities in the retinal vessels or retinal pigmented epithelium. Previous studies, using horseradish peroxidase in a primate model, suggested that leakage occurs primarily through this epithelium. This study was conducted to localize sites of the barrier breakdown in humans following different types of intra-ocular surgery and to compare them with eyes affected with ocular inflammatory disease, ocular infection, and choroidal melanoma. Paraffin sections of eyes were immunohistochemically stained for albumin to localize extravascular albumin, which was graded in a masked study. With aphakia/pseudophakia, penetrating keratoplasty, ocular inflammatory disease, ocular infection, and choroidal melanoma, barrier breakdown occurred primarily at the inner blood-retinal barrier (retinal vasculature), but leakage also occurred at the outer barrier (retinal pigmented epithelium). After retinal re-attachment surgery, the inner and outer blood-retinal barriers were equally compromised. Vascular leakage in the optic nerve head coincided with barrier failure in these disorders. The widespread pattern of blood-retinal barrier compromise with leakage at multiple sites suggests that soluble mediators are likely to play a role in postsurgical macular oedema, ocular inflammatory disease, and choroidal melanoma.

Albumins↗
PubMed2005

Risk and prognostic factors of poor visual outcome in Behcet's disease with ocular involvement.

PURPOSE: The purpose of the study was to determine factors correlated with the progression of irreversible visual disturbance in Behcet's disease (BD) with ocular involvement. METHODS: Forty-seven BD patients with ocular inflammation, who presented with the first ocular episode, and who had been followed continuously for 5-10 years in our hospital, were studied. Charts were reviewed for gender, onset age of uveitis, complete or incomplete type BD, HLA-B51 status, final visual acuity at the last remission period, mean number of ocular attacks per year, and clinical findings of iridocyclitis with profuse hypopyon, strong vitreous opacity blocking the observation of retinal vessels, diffuse retinal vasculitis, and exudates with hemorrhage within the retinal vascular arcade. RESULTS: Patients with a visual acuity of < or =20/200 and those with >20/200 differed significantly in the mean number of ocular attacks per year and clinical findings of strong vitreous opacity and exudates within the retinal vascular arcade, but not with regard to the other factors. In addition, the frequency of ocular attacks showed a significant negative correlation with the outcome of visual acuity. Logistic regression analysis indicated a significant association of an average of more than three ocular attacks per year, strong vitreous opacity, and exudates within the retinal vascular arcade with poor visual outcome. CONCLUSIONS: This study indicates that more than three ocular attacks per year, strong vitreous opacity, and exudates within the retinal vascular arcade are the risk and prognostic factors for a poor outcome of visual acuity in BD patients.

Adult↗
PubMedDate not supplied

Vitreous Hemorrhage.

The incidence of spontaneous vitreous hemorrhage is approximately 7 cases per 100,000 population. Proliferative diabetic retinopathy (32%), retinal tear (30%), proliferative retinopathy after retinal vein occlusion (11%) and posterior vitreous detachment without retinal tear (8%) are the most common causes of spontaneous vitreous hemorrhage. Vitreous hemorrhage can be caused by the pathologic mechanisms of disruption of normal retinal vessels, bleeding from diseased retinal vessels or abnormal new vessels, and extension of hemorrhage through the retina from other sources. Hemorrhage into the vitreous gel results in rapid clot formation and is followed by slow clearance of approximately 1% per day. The cellular response to vitreous hemorrhage is unusual with regard to hemorrhage in any tissue outside the vitreous cavity and has been compared to a "low-turnover" granuloma. Unique clinicopathologic features of long-standing vitreous hemorrhage include cholesterolosis bulbi (synchysis scintillans), hemoglobin spherulosis, and vitreous cylinders. Complications of nonclearing vitreous hemorrhage are hemosiderosis bulbi and glaucoma. Ghost cell glaucoma, hemolytic glaucoma, and hemosiderotic glaucoma may result from vitreous hemorrhage. The established treatment option for nonclearing vitreous hemorrhage is pars plana vitrectomy. Experimental nonsurgical treatment options involve improvement of physiologic clearance mechanisms in order to accelerate fibrinolysis, liquefaction, hemolysis and phagocytosis.

Animals↗
PubMed1994

Necrotic malignant melanoma of the choroid and concurrent intraocular manifestation of malignant non-Hodgkin's B cell lymphoma.

An 80-year-old white female developed clinical signs of a large choroidal malignant melanoma in her left eye. There were no signs of metastatic disease, but an asymptomatic chronic lymphatic leukemia was discovered. Histopathologic examination of the enucleated left eye showed a mostly necrotic malignant melanoma of the choroid with areas of spindle B cell differentiation, episcleral extension and secondary angle-closure glaucoma with necrosis of the anterior segment of the eye. On the basis of immunocytochemical studies of the lymphocytic infiltrates in the iridal blood vessels, retinal blood vessels and the choroid, the leukemic disease was classified as B cell lymphoma of low malignancy (lymphoplasmacytoid immunocytoma). A reactive T lymphocytic infiltration of the conjunctival stroma was also noted. Patients with malignant melanomas of the uvea require exclusion of a second malignancy.

Aged↗
PubMed1998

A new model of proliferative vitreoretinopathy.

PURPOSE: To design a new model of proliferative vitreoretinopathy (PVR) that would not rely on the addition of exogenous cells. The release of endogenous cells from surrounding attachments seems to be an early event in the pathogenesis of PVR. Because the proteolytic enzyme dispase dissociates tissues, the hypothesis was that an intraocular injection of dispase could trigger events that would cause PVR. The requirement for a surgical retinal break at the time of dispase injection was also examined. METHODS: One eye of Dutch Belted rabbits was injected with 0.003 U to 1.0 U dispase in the subretinal space or vitreous cavity. Control rabbits received a saline injection. An intentional retinal tear was created in animals in some groups. Observations were made for at least 10 weeks after surgery. RESULTS: Proliferative vitreoretinopathy developed in response to subretinal or intravitreal dispase, with or without creation of a controlled retinal break. Increased severity of PVR correlated with increasing doses of dispase. Evidence of PVR included preretinal membranes, distortion of myelin wings and retinal vessels, fixed retinal folds, and traction retinal detachment. Proliferative vitreoretinopathy did not develop in saline-treated control animals. CONCLUSIONS: Dispase initiated the development of PVR without the addition of exogenous cells, growth factors, or cytokines typically found in PVR membranes. A cascade of events was probably triggered by dispase, causing native cells and factors to produce PVR. The dispase model of PVR was technically easy to perform, permitted a clear view of the retina, and had a high success rate in development of PVR.

Animals↗
PubMed2002

Effect of sildenafil citrate (Viagra) on retinal blood vessel diameter.

PURPOSE: The present investigation was conducted to evaluate the effect of sildenafil citrate (Viagra, Pfizer Inc., New York, NY) on retinal blood vessel diameter. DESIGN: Double-blind randomized, placebo-controlled, cross-over study. METHODS: Fifteen healthy male volunteers (mean age 39 years) received 100-mg doses of sildenafil or matching placebo on 2 separate days. Monochromatic fundus photography was obtained in one eye, and brachial artery blood pressure and intraocular pressure were measured at baseline, 1 hour, and 5 hours after dosing. The diameters of two major temporal veins and one artery were measured in a masked fashion from digitized photographic negatives. RESULTS: In comparison with placebo, no statistically significant change in average venous diameter was observed for the superior (analysis of variance [ANOVA], P =.97), inferior retinal temporal vein (ANOVA, P =.73), or the retinal temporal artery (ANOVA, P =.89) after sildenafil treatment. In comparison to placebo, there was no significant difference in the percentage change from baseline in venous or arterial diameter at 1 or 5 hours after sildenafil. The power to detect a 6.5% change in retinal vascular diameter following sildenafil was approximately 80% (P =.05). CONCLUSIONS: These data suggest that at the maximum therapeutic dose used clinically (100 mg), sildenafil does not have a significant effect on retinal vascular caliber.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1993

[Mitral valve prolapse. A possible cause of retinal vascular occlusion in young patients].

Retinal vessel occlusion in the elderly is considered to be of arteriosclerotic etiology, but in young patients the reasons for retinal vessel occlusions are manifold and much more obscure. We report on five patients under the age of 45 years who had retinal artery occlusion or retinal vein obstruction. A detailed general investigation revealed nothing but an identical cardiac abnormality in all five cases: mitral valve prolapse (MVP). A potential explanation for the coincidence of retinal vessel occlusion and MVP might be local hyperaggregability of platelets generated by the prolapsing mitral valve. In conclusion, to prevent retinal vessel occlusion from recurring in patients with proven MVP, medication containing platelet aggregation inhibitors should be given.

Adult↗
PubMed1982

Presumed tuberculous maculopathy.

A solitary choroidal mass underlying the macula of a patient with active pulmonary tuberculosis involuted under antituberculosis therapy. Angiographic study revealed large blood vessels within the mass and secondary changes in overlying retinal vessels. These retinal vessels, despite their ophthalmoscopic configuration, had no demonstrable anastomosis with the vascular tree of the choroid.

Adult↗
PubMed1995

Local connected fractal dimensions and lacunarity analyses of 60 degrees fluorescein angiograms.

PURPOSE: The retinal vascular tree exhibits fractal characteristics. These findings relate to the mechanisms involved in the vascularization process and to the objective morphologic characterization of retinal vessels using fractal analysis. Although normal retinas show uniform patterns of blood vessels, in pathologic retinas with central vein or artery occlusions, the patterns are irregular. Because the generalized box fractal dimension fails to differentiate successfully between normal and abnormal retinal vessels in 60 degrees fluorescein angiograms, the authors have further investigated this problem using the local connected fractal dimension (alpha). METHODS: The authors studied 24 digitized 60 degrees fluorescein angiograms of patients with normal retinas and 5 angiograms of patients with central retinal vein or artery occlusion. The pointwise method estimated the local complexity of the angiogram within a finite window centered on those pixels that belong to the retinal vessels. Color-coded dimensional images of the angiograms were constructed by plotting the pixels forming the object with a color that corresponded to specific values of alpha +/- delta alpha. RESULTS: The color-coded representation allowed recognition of areas with increased or decreased local angiogram complexity. The alpha distributions showed differences between normal and pathologic retinas, which overcomes problems encountered when using the methods of calculating the generalized fractal dimensions. A multivariate linear discriminant function using parameters from the alpha distribution and a further fractal parameter--lacunarity--reclassified 23 of the 24 normal and 4 of the 5 pathologic angiograms in their original groups (total: 92.1% correct). CONCLUSIONS: This methodology may be used for automatic detection and objective characterization of local retinal vessel abnormalities.

Discriminant Analysis↗
PubMed1992

[Effects of endothelin on retinal blood vessels].

Endothelins (ETs), which are one of the most potent vasoconstrictors, were discovered in 1988. ETs are involved in the regulation of vascular smooth muscle and are thought to function like a local hormone. In this study, we measured changes in the caliber of retinal blood vessels caused by the intravitreal injection of ET 1 in rabbits, using fundus photography. The retinal artery showed an immediate vasoconstriction after the injection (0.1 ml) of ET 1 at 10(-6)M. However, ET 1 in lower concentrations (10(-7)M and 10(-8)M) caused vasodilations initially and subsequently vasoconstrictions. A dose-response relation was found. The blood vessel caliber reduced maximumly to 53% the value before injection. The vasoconstriction due to ET 1 may induce retinal ischemia and hypoxia. We speculate that ET 1 may be involved in the regulation of retinal blood vessels.

Animals↗
PubMed1990

Oxygen-induced retinopathy in the rat model.

Identification of a suitable animal model is essential for the continued study of retinopathy of prematurity (ROP). Since 1984 we have used the newborn rat for the study of oxygen-induced retinopathy (OIR). The rat retina is highly immature at birth. Like those of humans, the retinal vessels arise from mesenchymal precursors, but contrary to that which occurs in humans, canalization of the rats inner retinal vessels is not related to the presence of cystoid spaces. In addition, only immature Stage I photoreceptors are present around the optic disk at birth. This extreme immaturity makes the rat retina highly susceptible to direct damage from oxygen. Oxygen-induced retinopathy can be produced by exposing the newborn rat to 80% oxygen for the first 7-10 days of life. We have demonstrated that OIR does not develop when oxygen is administered under conditions of moderate hyperbarism (+1.8 atm). It is possible that hyperbarism exerts a protective effect on the immature retinal vessels by inducing a vasoconstrictive response which reduces the amount of oxygen transported from the choroid to the inner retina during hypoxia. I recently hypothesized that this vasoconstriction might also affect the ciliary body, thus reducing the quality of aqueous produced, and we are currently studying the relationship between development of the immature retinal vessels in the rat and production and drainage of the aqueous. The question we are attempting to answer is whether a condition of relatively increased intraocular pressure is capable of promoting the development of OIR.

Animals↗
PubMed2005

Retinal blood vessels develop in response to local VEGF-A signals in the absence of blood flow.

The role of hemodynamic forces and other signals from circulating blood in guiding the development of the retinal vasculature was examined by following the growth of these vessels in organ cultures. Retinal vascular development in organ cultures was monitored by immunofluorescent staining of retinal whole-mounts using antibodies against ICAM-2, a specific marker for endothelial cells and by vascular adenosine disphosphatase activity. Under culture conditions, the retinal vasculature from mice at postnatal day 3 (P3) grew from the optic nerve area to the edge of the retina in a manner similar to that observed in vivo. Both inner and outer vascular plexuses formed in retinal explants. Within the first few days of organ culture, the initial uniform meshwork of blood vessels was reorganized into arterioles, venules, and capillaries. As in animals, the initial retinal vascular plexus contained abundant vessels, and afterward some vessels regressed leading to the formation of a mature vascular bed. Changes in vascular density due to blood vessel growth and remodeling were confirmed by RT-PCR and Western blot analyses of ICAM-2 mRNA and protein levels, respectively. In addition, during in vitro retinal vascularization, arterioles acquired mural cell coverage, as shown by positive staining for alpha-smooth muscle actin. Thus, blood flow and blood-derived signals were not required for the development and maturation of retinal vessels. In contrast, stability of blood vessels in retinal explants was tightly regulated by endogenous levels of vascular endothelial growth factor-A (VEGF-A). VEGF-A was expressed in the explants throughout the culture period, and addition of neutralizing antibodies against VEGF-A to the organ culture caused a severe regression of blood vessels from the vascular front toward the optic nerve. In contrast, addition of anti-FGF-2 antibodies had no effect on the developing vasculature. Thus, retinal vascular development is dependent on local VEGF-A signals rather than systemic signals.

Actins↗
PubMed2001

Pseudoexfoliation syndrome in eyes with ischemic central retinal vein occlusion. A histopathologic and electron microscopic study.

PURPOSE: To determine histopathologically the prevalence of pseudoexfoliation (PEX) material in eyes enucleated secondary to ischemic central retinal vein occlusion (CRVO) and to evaluate eyes with PEX material in the anterior segment and CRVO ultrastructurally for PEX deposits in the vicinity of central retinal vessels. These deposits could explain an association of CRVO and PEX. METHODS: All surgically enucleated eyes with secondary angle closure glaucoma due to rubeotic iris secondary to ischemic CRVO (1981-1998) available were re-analyzed light microscopically for the presence of PEX in the anterior segment (n=120; 76.9+/-8.5 years [range: 51-91]). Eyes with PEX in the anterior segment and available optic nerve cross sections were examined by electron microscopy for PEX material in the retrolaminar (n=7) and intralaminar central retinal vessels (n=3). All eyes surgically enucleated because of malignant melanoma of the choroid aged 70 years and older (1981-1998) with sections available served as age-matched controls (n=107; 76.4+/-5 years [range: 70-91]). RESULTS: PEX material was present light microscopically in the anterior segment in 12 of 120 eyes with CRVO (10%) compared to 2 of 107 age-matched eyes with choroidal malignant melanoma (1.9%; p<0.05). Electron microscopically, neither structural alterations of the vessel wall nor PEX deposits were found in association with central retinal vessels both in the intra- and retrolaminar areas in any of the 7 eyes with PEX in the anterior segment and CRVO analyzed. CONCLUSIONS: Histopathologically, PEX is significantly more common in eyes enucleated secondary to CRVO compared to eyes enucleated because of an intraocular tumor. This most likely is due to the secondary open angle glaucoma in eyes with PEX as a known risk factor for CRVO. According to the small number of optic nerves analyzed here, there seems to be no morphologically evident PEX vasculopathy in the central retinal vessels both within and immediately behind the lamina cribrosa in eyes with PEX in the anterior segment and CRVO potentially causing retinal venous thrombosis.

Aged↗
PubMed1983

Falciform retinal fold as sign of familial exudative vitreoretinopathy.

We studied family members of 9 patients with falciform retinal fold, and found a number of cases showing features of familial exudative vitreoretinopathy (FEVR) in the fundi. Retinal fold was also seen in the eye of a cousin of the propositus. Three cases with falciform retinal fold were bilateral and 7 cases were unilateral. Retinal folds were located in the temporal half of the fundis in 11 of the 13 eyes with retinal fold. These 11 eyes showed avascularized zones of retinal vessels with scalloped edges in the periphery; in the 2 remaining eyes the retinal vessels were restricted within the fold. Thirty-one eyes of 18 cases, members of 7 pedigrees, showed features of FEVR. The observed avascularized zones with scalloped pattern of the vessels and vitreoretinal involvements were divided into 3 groups: 23 eyes of stage 1, 6 eyes of stage 2, and 2 eyes of stage 3, respectively. It was, therefore, concluded that falciform retinal fold being located temporally or bilaterally could be one of the signs of FEVR and that FEVR was a disease affecting regression of the hyaloid vascular system and development of the retinal vessels during fetal life. FEVR was classified into 4 groups: type 1, type 2, type 3 and type 4 of falciform retinal fold. The disease may be transmitted as autosomal dominant inheritance.

Adult↗