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At least 883 records · Page 49Linked to original sources
PubMed1984

Pathologic studies of the blood--retinal barrier in the spontaneously diabetic BB rat.

The BB rat spontaneously develops a diabetic state that closely resembles human type I diabetes. The authors studied the pathologic changes of the retina and retinal pigment epithelium of four normal and nine diabetic BB rats using (1) light and electron microscopy with the horseradish peroxidase tracer technique, and (2) trypsin digest preparations of the retinal vessels. They observed a retinal pigment epitheliopathy characterized by (1) derangement of the plasmalemma infoldings; (2) patchy organelle degeneration leading to focal necrosis; (3) increased permeability to horseradish peroxidase; and (4) repair of the pigment epithelium. Focal thickening of the retinal vascular basement membrane was seen occasionally, but the trypsin digest preparations were unremarkable. These studies suggest that diabetic retinal pigment epitheliopathy may be one of the early changes of diabetic retinopathy and may provide a pathogenetic mechanism for early disruption of the blood-retinal barrier.

Animals↗
PubMed2003

Online human conjunctival vessel diameter analysis. A clinical-methodical study.

BACKGROUND: The present study investigates the possible application of a commercially available on-line measuring device of retinal vessels for conjunctival vessel assessment. METHODS: Repeated measurements in one randomly chosen eye were performed in 11 healthy volunteers (mean age 42.9 +/- 10 years). Measurements of one conjunctival vessel were obtained first without a stimulus followed by measurements after the application of one drop of a topical vasoconstrictor. The examinations were performed by Retinal Vessel Analyzer (RVA, IMEDOS/Germany). This system determines automatically on-line the vessel diameter along a chosen vessel segment. RESULTS: Measurements in the native state without eye drop application showed an intraclass correlation coefficient of 0.97 and a mean variation coefficient of 1.8%. After application of the topical vasoconstrictor a short acting vasodilatation was observed with a magnitude of +10.9% +/- 14.9 (p < 0.001), followed by an increasing vasoconstriction (after 4 min -12.0% +/- 7.6; p = 0.004). One volunteer had no measurable conjunctival vessels in the baseline measurements and was therefore excluded from the study. DISCUSSION: The suggested technique allows the measurement of changes in conjunctival vessel diameter with high precision. The method represents a non invasive technique for the assessment of effects on conjunctival vessels caused by topical or systemic drugs.

Adult↗
PubMed2006

COX-2 protects against thrombosis of the retinal vasculature in a mouse model of proliferative retinopathy.

PURPOSE: Cyclooxygenases (COX-1 and COX-2) and prostaglandins regulate angiogenesis in several settings, including cancer and ischemia. In the eye, both selective inhibitors of COX-2 and nonselective COX inhibitors are reported to suppress ischemia-related retinal angiogenesis. Such studies however, may be confounded by the nonspecific effects of inhibitors. METHODS: Mice lacking either the COX-1 (COX-1(-/-)) or COX-2 isoform (COX-2(-/-)) were employed in a model of oxygen-induced retinopathy. Vascular responses were examined by histology, isolectin B4 staining of the abluminal endothelium, and retinal fluorescein angiography. RESULTS: There was an increase in intravitreal endothelial nuclei in hyperoxia-treated mice compared to normoxic controls irrespective of the genotype. Quantitative analysis of fluorescein-perfused and isolectin B4-stained retinal angiograms at postnatal day 18 (P18) revealed similar global levels of neovascular tufts in hyperoxia-treated wild-type, COX-1(-/-), and COX-2(-/-) mice. However, hyperoxia-treated COX-2(-/-) mice had increased areas of retinal nonperfusion (29.2+/-1.9 compared to 16.3+/-2.7; n=6; p<0.001). COX-1 disruption had no effect (15.6+/-2.6; n=8). Platelet deposition within retinal vessels was increased in hyperoxia-treated COX-2(-/-) mice (p<0.05). CONCLUSIONS: Genetic disruption of a single COX isoform is not sufficient to prevent oxygen-induced retinopathy. COX-2 protects retinal vessels from thrombosis, limiting the area of retinal nonperfusion in oxygen-induced retinopathy.

Animals↗
PubMed1980

Posterior ocular abnormalities after irradiation for retinoblastoma: a histopathological study.

Radiation-induced ocular lesions in the posterior eye and orbit were investigated in 33 surgical specimens of patients with retinoblastoma. The eyes were obtained from children 7 months to 6 years of age. Seventeen eyes were irradiated; 16 eyes had not received irradiation and served as controls. The majority of the irradiated eyes were treated with 6000 rads of external beam radiation. They were removed at a mean of 23 months after radiotherapy. All specimens were examined simultaneously by 2 observers without knowledge of treatment and analysed for the presence or absence of 15 lesions. The most consistent lesions in the irradiated eyes were abnormalities of the retinal vessels (11 of 17 eyes) and striking changes in the ciliary arteries (13 of 17 eyes). The retinal vessels showed thickening of the wall, often caused by deposition of fibrillary material, sometimes with fibrin deposits. The most consistent lesion was myointimal proliferation with narrowing of the ciliary arteries. Lesions of the central retinal artery were less common but occurred only in irradiated patients.

Child↗
PubMed1998

Retinal oxygen consumption during hyperglycemia in patients with diabetes without retinopathy.

OBJECTIVE: This study aimed to determine whether retinal oxygen consumption in patients with diabetes without retinopathy is affected by acute changes in blood glucose. DESIGN: The study design was a nonrandomized, interventional clinical study. PARTICIPANTS: The study consisted of 12 patients with diabetes without ophthalmoscopically visible diabetic retinopathy whose ages were 20 to 59 years (mean, 33.7 years). INTERVENTION: Retinal vessel oximetry was performed on subjects during normoglycemia and during acutely induced hyperglycemia. Hyperglycemia was achieved with the ingestion of an oral glucose load. MAIN OUTCOME MEASURES: Changes in retinal arterial and venous blood oxygen saturation resulting from systemic blood glucose changes were measured. Measurements were made using a noninvasive, two-wavelength digital imaging retinal vessel oximeter. RESULTS: In each subject, the measured retinal venous blood oxygen saturation decreased significantly during hyperglycemia. The amount of decrease in venous oxygen saturation associated with hyperglycemia was positively correlated with the duration of diabetes. The measured retinal arterial oxygen saturation did not change significantly during hyperglycemia. CONCLUSIONS: These results, taken with the observations of numerous other investigators that show increased blood flow during acute hyperglycemia, provide evidence of substantially increased retinal oxygen consumption during hyperglycemia. The results also complement previous observations of the effect of diabetes on retinal autoregulation.

Adult↗
PubMed2001

Confocal microscopic study of glial-vascular relationships in the retinas of pigmented rats.

Astroglia are interposed between the cerebral vasculature and neurons, where they may mediate the transfer of substances from the circulation to neurons and couple changes in neuronal activity to changes in cerebral blood flow. The retina is a particularly advantageous model system for studying glial-vascular interactions in situ. Confocal microscopy and three-dimensional image reconstruction were used to study the anatomical relationships between glia and the surface vasculature in retinas acutely isolated from adult pigmented rats. Retinas were immunostained using antibodies directed against the basal lamina surrounding the vasculature as well as antibodies directed against glial fibrillary acidic protein. Surface vessels of all calibers were contacted by the processes of astrocytes. The vitreal surfaces of the large retinal vessels were covered by a meshwork of immunoreactive astrocyte processes of a variety of shapes, whereas the scleral surfaces of the vessels were supported by thick bundles of astrocyte processes. In addition, glial cells were filled intracellularly with the gap junction-permeable tracers Lucifer yellow and Neurobiotin. Intracellular fills clearly demonstrated the presence of astrocytes with somata that were closely apposed to the large retinal vessels. Tracer-filled astrocytes displayed a variety and complexity of shapes that was not apparent in immunostained material. Gap junctional coupling was stronger between astrocytes adjacent to the same artery than between periarterial astrocytes and astrocytes located away from arteries. Significantly fewer Müller cells were labeled when Neurobiotin was injected into astrocytes associated with arteries than when Neurobiotin was injected into astrocytes that were distant from arteries.

Animals↗
PubMed1998

[Flicker stimulation induces retinal vasodilation in man].

BACKGROUND: Previous studies have demonstrated, in the cat, a vasodilatation of retinal vessels in response to neuronal activity induced by diffuse luminance flicker. The aim of this study was to determine whether a similar diameter variation is detectable in humans. MATERIALS AND METHODS: Nine normal subjects were exposed to 1 min of sinusoidally varying diffuse luminance flicker (10 Hz, 30 degrees around optic nerve head). Monochromatic fundus pictures before and after the stimulation were taken. The diameter of retinal arteries and veins was measured on the digitised photographs with the NIH-Image software and an own algorythm. RESULTS: The diameter immediately after flicker was significantly larger than the pre-stimulus diameter by 4.2 +/- 2.2% (p < 0.014) (mean +/- SD) for the retinal arteries and 2.7 +/- 1.7% (p < 0.001) for the retinal veins. Six seconds after cessation of the flicker, arterial diameter was not significantly different from that of pre-flicker value. CONCLUSIONS: Diffuse luminance flicker induces an increase in retinal vessel diameter. This suggest that retinal blood flow is coupled with neuronal activity as previously evidenced by the blue field simulation technique in the macula.

Adolescent↗
PubMed1980

The rationale of photocoagulation therapy for proliferative diabetic retinopathy: a review and a model.

A model is proposed for initiation and inhibition of growth in retinal vessels including the control of proliferative diabetic retinopathy by photocoagulation. The model assumes that chronic dilatation (constriction) of a retinal blood vessel causes (inhibits) growth. Destruction of rods and cones by photocoagulation allows more choroidal oxygen to reach the inner retina and constrict retinal vessels. The attenuated vessels in late stage retinitis pigmentosa are an analogous and exaggerated effect to that from photocoagulation. The control of proliferative diabetic retinopathy is compared to the cause of retrolental fibroplasma. Following vitrectomy the retina utilizes oxygen from the aqueous which results in dilatation of iris vessels followed by rubeosis iridis. From this model, neovascularization from the disc or angle vessels follows the dilatation resulting from increased flow in their distal vascular beds.

Diabetic Retinopathy↗
PubMed1994

Blood-eye barriers in the rat: correlation of ultrastructure with function.

The function of different vascular beds in the rat eye and brain was evaluated by measuring the transfer of a vascular tracer, 14C-alpha-amino-isobutyric acid, from blood to tissue. The density of vascular pores was measured in electron micrographs of perfusion-fixed, age-matched tissue to determine whether the differences in tracer transfer were paralleled by differences in ultrastructure. Tracer transfer in retina was approximately four times that in brain of the same animal. The transfer constant was not changed by the inclusion of cold alpha-amino-isobutyric acid, showing that transport across retinal vessels is not saturable, and indicating that, as in brain, transport is due to passive diffusion. Ultrastructurally, retinal vessels have a higher density of interendothelial junctions and of endothelial vesicles, both of which suggest higher vascular permeability. However, pericytes, which contribute to a second line of defence in the blood-brain barrier, are approximately four times as numerous in retina as in brain, and we suggest that in the retina, they act to compensate for a more permeable endothelial barrier. Ciliary body vessels had a high transfer of tracer, probably as a consequence of the fenestrations in their walls. Iridial vessels had a relatively low transfer of tracer, similar to that in retina even though a proportion of the interendothelial junctions in iridial vessels had expanded junctional clefts suggestive of open paracellular channels. However, both iris and ciliary body may lose tracer to the anterior chamber fluid, leading us to underestimate the vascular permeability in these sites.

Aminoisobutyric Acids↗
PubMed2003

Change in endothelial nitric oxide synthase in the rat retina following transient ischemia.

Patterns of endothelial nitric oxide synthase (eNOS) expression in retinal ischemia were studied utilizing a transient high intraocular pressure (HIOP) model. We investigated neuronal cell damage and changes in eNOS immunoreactive expression in the ischemic retina, and its relationship to the neuroprotection of betaxolol treatment after ischemic injury. Immunohistochemical staining for eNOS was performed at 3, 7, 14 and 28 days after ischemia/reperfusion. In controls, eNOS immunoreactivity was detected in retinal vessels, but was not detected in neurons. After ischemia/reperfusion, the intensity of eNOS immunoreactivity increased in both retinal vessels and the ganglion cell layer (GCL) compared with controls. eNOS-positive neurons were induced first in the inner nuclear layer (INL) 7 days after reperfusion. However, when experiments were carried out on animals that had been treated with betaxolol after ischemia/reperfusion, the intensity of eNOS immunoreactivity decreased compared to the untreated ischemic retinas. These results suggest that an increase in eNOS expression could be associated with the degenerative changes in the ischemic retina, and that betaxolol treatment appears to protect retinal tissue from ischemic damage.

Administration, Topical↗
PubMed1978

The effect of blood on ocular fundus reflectance and determination of some optical properties of retinal blood vessels.

Light reflected from 50 micrometer diameter spots on the fundi of two adult rhesus monkeys was measured as a function of wavelength in 10 nm jumps from 400 to 900 nm. The areas measured were a retinal artery and vein, areas of the disk, macula, and retina devoid of visible blood vessels, and the foveola. The eyes of the two monkeys were then exsanguinated, the blood vessels were filled with normal saline, and reflectances of the same spots on the fundi were again measured. The pairs of reflectance curves were compared and demonstrated that blood is not the major determinant of the characteristic shapes of the retinal tissue spectral reflectance curves. From the pre-exsanguination and postexsanguination data, the isolated retinal artery and vein wall reflectances were determined to be 0.020 and 0.009, respectively, their transmittances 0.837 and 0,977, and the fractions of light absorbed by them 0.143 and 0.014, respectively, in the visible spectral region below 500 nm.

Animals↗
PubMed2000

Reduced expression of the adherens junction protein cadherin-5 in a diabetic retina.

PURPOSE: Transvascular leakage occurs in diabetic retinopathy. The tight junction proteins occludin and zonula occludens-1 (ZO-1) and adherens junction protein cadherin-5 are critical to the maintenance of endothelial barrier. We report a comparison of junction protein expression in the normal and diabetic retina. METHOD: Case report. Postmortem retinal cryosections were prepared from the left eye of a 73-year-old woman with diabetic retinopathy. Cryosections were immunostained for cadherin-5, occludin, and ZO-1 and compared with retinal cryosections from the right eye of a 72-year-old man with no progression of retinal disease. RESULTS: Immunofluorescence showed positive retinal vessel staining for occludin and ZO-1 in both eyes and cadherin-5 in the normal eye but reduced cadherin-5 staining in the retinal vessels of the diabetic eye. CONCLUSION: Increases in transvascular leakage observed in diabetic retinal vasculature may be associated with reduction in the expression of the critical adherens junction protein, cadherin-5.

Aged↗
PubMed1979

[Vascular anastomoses at the posterior pole of the eye (author's transl)].

Anastomoses between vessels of the fundus may occur as congenital malformations or secondary to vascular diseases affecting the eye. Congenital anastomoses can be of the racemose hemangioma type, with severe malformation of the retinal vessels, ocular complications, and neurologic manifestations, or as simple A-V shunts with visual impairment but limited tendency to show other ocular or neurologic involvement. These anastomoses must be distinguished from other vascular malformations like telangiectasis (Leber, Coats) or the angiomatous lesions of von Hippel's disease. Secondary anastomoses may be confined to the retinal vessels or involve chorioretinal connections. Retinal anastomoses occur in vascular disorders like retinal vein occlusions, diabetes, periphlebitis and hemoglobinopathies. They are often amenable to treatment by light coagulation. Chorioretinal anastomoses occur whenever Bruch's membrane is destroyed by traumatic, inflammatory, degenerative or physical (light coagulation) influences. Light coagulation may be the appropriate treatment, although complications are not rare.

Adolescent↗
PubMed1995

Angioscotomata and morphological features of related vessels in automated perimetry.

AIMS: To determine principles which regulate the occurrence of angioscotomata in automated static perimetry, variations in light sensitivity were correlated with the location and diameter of neighbouring retinal vessels. METHODS: Ten normal eyes were tested with the Octopus 2000R, using a 0.431 degree light stimulus. Sensitivity was quantified in points located around the blind spot, according to a regular, 0.5 degree constant, grid pattern. From 336 to 443 locations were tested in each eye. The resulting printouts were superimposed on corresponding fundus photographs. At each tested point, the following five additional variables were evaluated: the diameters of the closest and the second closest vessel (in 0.1 degree units); the distances of the apparent location of the tested point to the closest and the second closest vessel (in 0.25 degree units); and the distance between the two closest vessels (in 0.25 degree units). Altogether, 3869 locations were tested and 23,214 values were quantified. RESULTS: The following two conditions were found to be related to a reduction in sensitivity: (1) proximity (< 0.25 degree) to a large vessel (> or = 0.5 degree in diameter); (2) proximity (< 0.25 degree) to one of two adjacent (< 0.5 degree distant), moderately large vessels (0.3 degree to 0.4 degree in diameter). In condition 1, sensitivity was 51.3% and specificity was 92.2%; in condition 2, sensitivity was 16.2% and specificity was 98.3%; and with a combination of conditions 1 and 2, sensitivity was 67.6% and specificity was 90.5%. Increase by 0.1 degree of an adjacent vessel which was 0.4 degree in diameter markedly affected light sensitivity. CONCLUSION: Modifications in vessel diameter are observed in a number of circumstances, including adaptive vascular response to changes in ambient conditions and obstructive disorders of retinal vessels. These findings indicate that changes in vessel diameter over time can result in fluctuation of sensitivity. It is concluded that, in contrast with what is commonly stated, when ocular media are unaltered and the subject's collaboration is adequate, temporal variations in measured thresholds do not necessarily reflect functional changes in nervous tissues in the visual pathways.

Adult↗
PubMed1976

The retina in type 5 hyperlipoproteinemia.

Of two patients with type 5 hyperlipoproteinemia, one exhibited lipemia retinalis with multiple retinal hemorrhages and intraretinal lipid extravasations. Postmortem examination showed hemorrhages in the inner retinal layers and lipid deposits largely in the outer plexiform layer. Lipid within the walls of the retinal vessels was demonstrated by light and electron microscopy. The second patient exhibited visual loss due to progressive obstruction of retinal vessels with white material presumed to be lipid. Findings were confined to one eye.

Adult↗
PubMed1995

[Ocular findings in Desferal therapy].

Desferrioxamine (DFO) is the most important drug in the treatment of thalassemia major and other hematological diseases requiring regular transfusion. It eliminates excessive ferritin by building up chelate complexes. Different mechanisms of possible DFO toxicity are induction of oxidation, damage of the blood-retina barrier, or reduction in other metalloions (Cu2+, Zn2+). The objective of the present study was to evaluate the ocular side effects of DFO treatment. We prospectively examined 17 patients aged 5 to 25 years, all of them treated with DFO. Visual acuity, pupillary reaction, anterior segment, lens and fundus were checked. If possible, visual fields, color vision, dark adaptation, stereoscopic vision, and contrast sensitivity were investigated. Lens opacities were found in 41% (7/17), changes in the retinal pigment epithelium in 35% (6/17), tortuosity of retinal vessels in 24% (4/17), dilation and sheathing of the retinal vessels in 18% (3/17), defects in color vision in 29% (5/17), and abnormal dark adaptation in 18% (3/17) of the patients. The oculotoxicity of DFO is dose-dependent. Major side effects like depression of the visual acuity are partially reversible after discontinuing the therapy. Regular ophthalmological check-ups are therefore necessary.

Adolescent↗
PubMed2006

Hyperviscosity-related retinopathy in waldenstrom macroglobulinemia.

OBJECTIVES: To determine the earliest retinal changes associated with Waldenström macroglobulinemia (WM) and to ascertain the serum IgM and serum viscosity (SV) levels at which these changes occur. METHODS: Patients with WM were evaluated using indirect ophthalmoscopy with scleral depression, laser Doppler retinal blood flow measurements, and serum IgM and SV determinations. Hemodynamic findings were compared with those of a group of age-matched controls. A retinopathy severity scale was developed, and the associated IgM and SV values were related to particular morphologic changes. RESULTS: A total of 46 patients with WM and 14 age-matched, healthy controls participated in the study. Patients exhibited far-peripheral hemorrhages and venous dilation with increasing SV and IgM values. Central retinal changes were associated with significantly higher SV values. Retinal vessel diameter increased with increasing serum IgM and SV levels. The mean IgM level of patients with the earliest retinal changes was 5442 mg/dL. The mean SV level was 3.1 cP. CONCLUSIONS: Retinal manifestations of hyperviscosity syndrome occur at lower serum IgM and SV levels than previously reported. Indirect ophthalmoscopy with scleral depression along with retinal vessel diameter measurements are able to detect the earliest hyperviscosity syndrome-related complications and should be considered in the treatment of patients with WM.

Blood Flow Velocity↗
PubMed1983

[Measurement of flow physiology of the large vessels in retinal circulation in type 1 and type 2 diabetics].

Segmental blood flow, velocity, and vessel diameter were measured in 21 eyes of diabetic individuals with diabetes type 1 and 2. The results for arterial blood flow, velocity, arterial and venous vessel diameter in diabetes show significant differences from the results measured in normal individuals. These flow magnitudes, excluding arterial diameter, significantly depend on the duration time of diabetes. The retinal blood flow magnitudes alter before the marks of diabetic retinopathy are visible. There are differences between the results in diabetes type 1 and type 2 regarding dependence on the duration time of diabetes.

Adolescent↗