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At least 1,117 records · Page 62Linked to original sources
PubMed2001

Functional imaging of the retinal microvasculature by scanning laser Doppler flowmetry.

PURPOSE: to image functionally perfused retinal vessels and to assess quantitatively the intercapillary space of the retinal microvasculature. METHOD: The base of functional imaging and the quantitative assessment of the retinal vasculature is the two-dimensional map of the retina encoded by the laser Doppler frequency shift. By Scanning Laser Doppler Flowmetry (HRF. Heidelberg Engineering) the laser Doppler frequency shift of 16.384 retinal sites (256 pixels x 64 lines, spatial resolution 10 mum) of a retinal area of 2.7 x 0.7 mm was gained. The image processing was performed by a recently described algorithm (AFFPIA). Using the data of the laser Doppler frequency shift of every retinal site, a color-coded retinal image was established showing perfused vessels and capillaries. By automatic pattern analysis of this image vessels and capillaries were identified and segmented. Based on this image the distances in [microm] of every retinal site to the next vessel or capillary were calculated ("distance to next capillary"). The functional imaging of the retinal perfusion was demonstrated in (1) normal retina, (2) retinal arterial occlusion, and (3) proliferative retinopathy. Intraobserver reliability of the quantitative assessment of the parameter "distance to next capillary" was estimated by measuring 10 eyes of 10 subjects at 5 different days by one observer. Interobserver reliability of the quantitative assessment was evaluated by analysing 10 perfusion maps by 5 different operators. In 93 eyes of 71 normal subjects (mean age 40.4 mu 15 years) the juxtapapillary retina was quantitatively evaluated. RESULTS: QUALITATIVE EVALUATION: The functional images of the retinal perfusion of eyes with normal retina, with retinal arterial occlusion, and with proliferative retinopathy corresponded well with the fluorescein angiography. Perfused vessels and capillaries became visible in a high local resolution. QUANTITITATIVE ASSESSMENT: The coefficient of reliability of the introobserver and interobserver reproducibility of the parameter 'mean distance to next capillary" was 0.74, and 0.95, respectively. The quantitative assessment of the perfusion showed that the major part of the retinal sites (>700%) had distances to the next capillary lower than 30 microm 46% of the retinal area had distances to the next capillary from 0-20 microm 26% of the retina had distances from 20-30 microm, 12% of the retina had distances from 30-40 microm 7% of the retina had distances from 40-50 microm, 4% of the retina had distances from 50-60 microm, and 4% of the retinal sites showed distances to the next capillary greater than 60 mum. The mean distance to the next capillary or vessel was calculated with 21 +/- 6.5 microm. CONCLUSION: By non-invasive Scanning Laser Doppler Flowmetry in combination with adequate software it is possible to perform a functional imaging of the retinal vasculature and to measure all index for the functional density of retinal capillaries and vessels.

Adult↗
PubMed1996

Intravitreous injections of vascular endothelial growth factor produce retinal ischemia and microangiopathy in an adult primate.

PURPOSE: The purpose of the study is to determine the effect of exogenous vascular endothelial growth factor (VEGF) on the primate retina and its vasculature. METHODS: Ten eyes of five animals were studied. Physiologically relevant amounts of the 165 amino acid isoform of human recombinant VEGF were injected into the vitreous of six healthy cynomolgus monkey eyes. Inactivated human recombinant VEGF or vehicle was injected into four contralateral control subject eyes. Eyes were assessed by slit-lamp biomicroscopy, tonometry, fundus color photography, fundus fluorescein angiography, light microscopy, and immunostaining with antibodies against proliferating cell nuclear antigen and factor VIII antigen. RESULTS: All six bioactive VEGF-injected eyes developed dilated, tortuous retinal vessels that leaked fluorescein. Eyes receiving multiple injections of VEGF developed progressively dilated and tortuous vessels, venous beading, edema, microaneurysms, intraretinal hemorrhages and capillary closure with ischemia. The severity of the retinopathy correlated with the number of VEGF injections. None of the four control eyes exhibited any abnormal retinal vascular changes. The endothelial cells of retinal blood vessels were proliferating cell nuclear antigen positive only in the bioactive VEGF-injected eyes. CONCLUSION: Vascular endothelial growth factor is sufficient to produce many of the vascular abnormalities common to diabetic retinopathy and other ischemic retinopathies, such as hemorrhage, edema, venous beading, capillary occlusion with ischemia, microaneurysm formation, and intraretinal vascular proliferation.

Animals↗
PubMed1996

The relation between expression of vascular endothelial growth factor and breakdown of the blood-retinal barrier in diabetic rat retinas.

In the retinas of streptozotocin-induced diabetic rats, the relationship between the expression of vascular endothelial growth factor (VEGF) and the breakdown of the blood-retinal barrier (BRB) was investigated. VEGF mRNA expression was examined by in situ hybridization and VEGF protein expression was examined by immunohistochemistry. BRB breakdown was immunohistochemically demonstrated by detecting extravasation of albumin. In diabetic retinas, VEGF mRNA was expressed by the following cells: (a) ganglion cells, (b) glial cells such as astrocytes and Muller cells, whose cell processes are closely associated with retinal vessels, (c) smooth muscle cells and pericytes in the vessel walls, and (d) the retinal pigment epithelium. In diabetic retinas, BRB breakdown was immunohistochemically detected, and VEGF protein expression was markedly increased in comparison to that in the control retinas. The rates of both BRB breakdown and VEGF immunoreactivity increased in proportion to the duration of diabetes. In addition, the rate of BRB breakdown was much higher in vessels with VEGF immunoreactivity than in vessels without VEGF immunoreactivity. These findings indicate that VEGF has a major promoting effect on BRB breakdown in simple diabetic retinopathy. VEGF immunoreactivity was distributed throughout all layers of the retinas, and were most prominently observed in the nerve fiber layer, especially near the optic disc and around large vessels. These two regions coincide with the sites wherein BRB breakdown is clinically detected by fluorescein angiography in diabetic patients. Neovascularization in proliferative diabetic retinopathy is also most commonly observed in these two regions. Because VEGF promotes endothelial proliferation, these findings suggest that VEGF plays a role in the budding of retinal neovascularization and, as a result, could induce proliferative diabetic retinopathy.

Animals↗
PubMed1980

Experimental inflammatory serous detachment of the retina.

Rhesus monkey eyes were studied after the development of inflammatory serous retinal detachments following internal carotid artery injection of live, yeast-phase Histoplasma capsulatum organisms. Horseradish peroxidase (HRP) was used as a tracer to examine the inner and outer blood-retinal barriers. The HRP was present in a decreasing gradient from the choroid into the subretinal space and was not found to have leaked from retinal vessels. The source of subretinal fluid in this model of inflammatory serous retinal detachment was leakage from the choroid through a defective outer blood-retinal barrier, induced by disruption of the retinal pigment epithelium. This model has relevance to understanding the serous retinal detachments common to diseases affecting the choroid.

Animals↗
PubMed2002

Lipid hydroperoxide stimulates leukocyte-endothelium interaction in the retinal microcirculation.

Leukocyte dynamics were evaluatyed in vivo in rat retinal microcirculation following exposure to lipid hydroperoxide (LHP) in the vitreous.Various amounts (1, 5, 10 or 100 microg) of LHP (18:2) dissolved in 5 microl of sodium borate buffer (SBB, 0.02M) were injected into the vitreous of Brown-Norway rats. As a comparative study, 10 microg of linoleic acid (LA) dissolved in 5 microl of SBB was injected in the same way. Rats that did not undergo injection were evaluated as un-treated. At 2 to 48 hr after LHP exposure, the following were examined: (1) the flux of rolling leukocytes along the major retinal veins, (2) the number of leukocytes that accumulated in the retinal microvasculature using acridine orange digital fluorography and (3) the diameter of major retinal vessels. In the LHP-treated eyes, leukocyte rolling along the major retinal veins was observed and the number increased in a dose-dependent manner ( 1 to 10 microg). The flux of rolling leukocytes peaked at 6 hr after LHP (10-100 microg) injection. No rolling leukocytes were observed in LA-treated or un-treated eyes. The number of accumulated leukocytes started to increase at 4 hr and peaked at 24 hr after LHP (10 microg) injection. This number was significantly higher than that in LA-treated and un-treated eyes. Venous dilation was seen from 4 hr after LHP (10 microg) injection and became significant at 6 and 24 hr as compared with LA-treated and un-treated eyes. The results indicate that increased LHP levels in the vitreous due to oxidative stress enhance leukocyte-enothelium interaction in the retinal microcirculation.

Animals↗
PubMed2005

Developmental abnormalities in the Nuc1 rat retina: a spontaneous mutation that affects neuronal and vascular remodeling and retinal function.

The retina serves as an excellent model in which to study vertebrate CNS development. We have discovered a spontaneous mutation in the Sprague-Dawley rat that results in a novel and unusual ocular phenotype, including retinal abnormalities, that we have named Nuc1. We have previously shown that the Nuc1 mutation appears to suppress programmed cell death in the developing retina. Here we report that maturation of both the retinal neurons and the retinal vessels is abnormal in Nuc1 homozygous rats. The developmental changes in the retinal neurons and vasculature are correlated with regard to degree of abnormality. As Nuc1 homozygotes mature, focal retinal detachment begins at approximately 3 months after birth, and near total traction retinal detachment, associated with pre-retinal fibrosis and neovascularization, is evident by 18 months. Electroretinographic studies at 2.5 months of age indicate that functional retinal degeneration precedes retinal detachment. The functional abnormality is most evident in rods and the inner retina, and is present in homozygous but not heterozygous mutants. Immunocytochemical studies of rod and cone photoreceptors indicate abnormalities in rod, but not cone, photoreceptors in Nuc1 homozygotes, consistent with the electroretinographic findings. In Nuc1 animals, the Muller cells are activated. Although such activation may result from inflammation, Muller cells in Nuc1 may be reacting to a neuronal influence. It appears that the Nuc1 mutation plays a regulatory role in both developing and maturing ocular tissues. The Nuc1 mutation may also serve as an important genetic tool to explore the relationships that may exist among gliosis, normal neuronal development, and normal vascular development and how abnormalities in these associations lead to common retinal diseases.

Amacrine Cells↗
PubMed2003

Accumulation of neurocan, a brain chondroitin sulfate proteoglycan, in association with the retinal vasculature in RCS rats.

PURPOSE: To examine whether and how the retinal distribution of the chondroitin sulfate proteoglycan neurocan is affected after photoreceptor cell loss and whether it correlates with the multiple secondary cellular changes that accompany the photoreceptor degeneration. METHODS: Retinas from normal rats (Sprague-Dawley; postnatal days [P]0-P70), RCS rats with dystrophic retinas (P0-P300), RCS-rdy(+) congenic rats with nondystrophic retinas (P0-202), and rhodopsin mutant rats, P23H (P0-P257) and S334ter (P0-P220), were processed for immunohistochemistry using a polyclonal antibody to rat neurocan. RESULTS: The overall distribution of neurocan was similar in all retinas examined. Neurocan immunostaining was detected over the nerve fiber layer, the plexiform layers, the photoreceptor outer segments region, and the ciliary epithelium. With age, labeling throughout the plexiform layers decreased continuously. In RCS rats however, conspicuous labeling was also seen in association with retinal vessels, from P15 onward. CONCLUSIONS: Accumulation of neurocan in association with the retinal vasculature does not correlate with photoreceptor cell loss, because it was not observed in the rhodopsin mutant rats. During the earliest stages of the disease, accumulation of debris in the subretinal space in RCS rats may be sufficient per se to initiate a cascade of metabolic changes that result in accumulation of neurocan. With time, the neurocan accumulated perivascularly may, by interaction with other matrix molecules, modulate at least some of the vascular alterations observed in this animal model.

Animals↗
PubMed2003

Enhanced recombinant adeno-associated virus-mediated vascular endothelial growth factor expression in the adult mouse retina: a potential model for diabetic retinopathy.

Diabetic retinopathy, one of the most serious complications of long-term diabetes, could clinically be divided into two stages: 1) background retinopathy that does not cause visual impairment and 2) proliferative retinopathy, which is a potentially blinding condition. This study aims to investigate the correlation between enhancement of vascular endothelial growth factor (VEGF) expression and neovascular changes. A binary recombinant adeno-associated virus construct producing green fluorescent protein (GFP) and VEGF under the control of the human cytomegalovirus promoter, recombinant adeno-associated virus (rAAV).VEGF.GFP, was produced and injected into the subretinal space of C57BL mice. GFP expression was tracked by fluorescence fundus photography, and VEGF expression was confirmed by immunohistochemistry and enzyme-linked immunoassay. Neovascular changes were monitored by fluorescein angiography and histology and by quantifying the number of inner retinal vessels. GFP expression was found in 100% of injected eyes, and vascular changes were detected in 9 of 10 rAAV.VEGF.GFP-injected eyes. Of these, four demonstrated microaneurysms and five showed moderate to severe leakage. There was a statistically significant increase in blood vessel number in the inner nuclear layer (P < 0.03) and dilatation of retinal veins (P < or = 0.05). This work has demonstrated that the development of different stages of diabetic retinopathy is closely correlated with an increased VEGF level in the retina.

Animals↗
PubMed1980

Parafoveal retinal telangiectasis. Light and electron microscopy studies.

The clinical, histopathological, and ultrastructural features of a case of parafoveal telangiectasis are reported. No telangiectasis of retinal vessels was found. Instead, there was thickening of the wall of the retinal capillaries and narrowing of the calibre of the lumen. Thickening was due to marked proliferation of basement membrane in a multilayered configuration, Cellular debris from degenerated endothelial cells and pericytes, and multimembranous lamellar lipid material were entrapped between layers of basement membrane. Extensive degeneration of pericytes was observed, and occasional areas showed degenerated endothelial cells. These changes were not restricted to the clinical-affected parafoveal area but were also seen to a lesser degree throughout the retina. The changes are interpreted as being due to primary endothelial cell degeneration and regeneration, with successive waves of basement membrane production and secondary degeneration of pericytes.

Basement Membrane↗
PubMed1991

Alterations in glial cell morphology and glial fibrillary acidic protein expression in urethane-induced retinopathy.

Urethane injection in newborn rats causes a photoreceptor degeneration without initial damage to the retinal pigment epithelium, choriocapillaris, or inner retina. In later stages, retinal vessels become incorporated into the retinal pigment epithelium (RPE) and change from a continuous endothelial cell phenotype to a fenestrated phenotype. At the light-microscopic level, there do not appear to be morphologic changes in the inner retina up to 24 weeks of age. Ultrastructurally, however, there are alterations in Müller cell cytotopographic organization. In the normal retina, intermediate filaments are primarily found from the ganglion cell layer to the inner nuclear layer. These filaments do not show glial fibrillary acidic protein immunoreactivity (GFAP-IR) in the normal animal. In the urethane-treated animals, the compartmental organization of the Müller cell organelles is moved vitread. Intermediate filaments are found in the end-foot region, and in the inner plexiform layer, bundles of intermediate filaments become more prominent. All of these filaments are GFAP-IR positive. The new expression of GFAP in the Müller cell may be linked to the observed rearrangement of the cytoskeletal elements. In urethane-induced retinopathy, GFAP-IR is found associated with vessels in all layers of the remaining retina. However, it is not seen accompanying vessels into the RPE. Ultrastructurally, there is no glial investment of the RPE-associated vessels. This absence of glial investment may permit the change in phenotype observed in these vessels.

Animals↗
PubMed1964

THE PRESENT STATUS OF RETROLENTAL FIBROPLASIA.

The incidence of retrolental fibroplasia in premature babies has been greatly reduced since the curtailment of oxygen concentration and exposure time. However, in infant care, cases still occur in premature infants who have respiratory distress and cyanosis. The incidence is lowest where oxygen in excess of 40 per cent is never administered, regardless of the status of the infant. The mechanism by which oxygen causes obliteration of retinal vessels has not been discovered. A sampling of teaching institutions revealed that more than 30 cases have been seen since 1959.

Cyanosis↗
PubMed1983

Platelet-fibrin embolism in a rhesus macaque: angiographic and pathologic studies comparing fluorescein and indocyanine green.

A male rhesus macaque was found to have what appeared to be numerous platelet-fibrin emboli in retinal vessels in the perimacular area. Indocyanine green (ICG) dye fluorescence and fluorescein angiograms of the fundus demonstrated leakage of fluorescein, but not ICG, from the involved arterioles. Histopathologic changes in the eyes included occlusion of retinal and choroidal vessels with platelet-fibrin emboli, inner retinal ischemia, ischemic injury to the parafoveal capillary bed distally to occlusion of precapillary arterioles, and retinal exudate limited to the regions of capillary damage. Differential leakage of fluorescein may be explained by the difference in binding affinities of the 2 dyes to blood protein: 20% to 40% of the circulating fluorescein is unbound, and 98% of ICG is bound to serum albumin. Simultaneously or serially performed angiograms with fluorescent probes of different sizes might be used to obtain a qualitative measure of vascular integrity in persons with embolism, diabetic retinopathy, sickle cell retinopathy, vasculitis, and other disorders known to produce focal retinal and choroidal vascular occlusion.

Animals↗
PubMed1987

Effects of beta-agonists on b- and c-waves implicit for adrenergic mechanisms in cat retina.

Nylidrin (buphenine) is a beta-adrenergic agonist known to dilate peripheral vessels and used therapeutically in retinal degeneration and glaucoma. We studied retinal function under beta-agonists in arterially perfused cat eyes and observed a dose-dependent, reversible increase in b-wave amplitude and a decrease in c-wave amplitude in concentrations from 4.5 to 120 microM. A half maximal response was obtained at 40 to 50 microM. The optic nerve response to light showed dose-dependent reversible changes under nylidrin. Standing potential, light peak, intraocular pressure, vascular resistance, and diameter of or retinal vessels showed no consistent changes under nylidrin. The effect were inhibited by each of the beta-blocking agents propranolol, ICI 118, and oxprenolol (in sequence of decreasing potency). Another potent beta 2-agonist, clenbuterol, was used to determine the extent to which the responses to nylidrin were due to beta-receptor-mediated action. Clenbuterol had similar effects on the b-wave and optic nerve response at slightly higher concentrations (30 200 microM) but more variable effects on the c-wave. The data are interpreted as functional evidence that beta-adrenergic mechanisms are involved in retinal signal processing. This concept is corroborated by identification of beta-adrenergic binding sites in cat retina (Bruinink et al., 1986).

Adrenergic beta-Agonists↗
PubMed2004

Cardiovascular disease, mortality, and retinal microvascular characteristics in type 1 diabetes: Wisconsin epidemiologic study of diabetic retinopathy.

BACKGROUND: Diabetic retinopathy and proteinuria, manifestations of microvascular abnormalities, occur early in the course of diabetes mellitus; in contrast, macrovascular cardiovascular complications usually occur later. Retinal vessel characteristics may be informative about risk of cardiovascular disease in persons with diabetes. We evaluated this in a longitudinal cohort study of persons with type 1 diabetes. METHODS: The population consisted of persons with type 1 diabetes who were receiving care in 11 counties in Wisconsin. Subjects (n = 996) were examined at baseline (1980-1982), and 4, 10, 14, and 20 years later. Evaluations included medical history and measurements of height, weight, blood pressure, and glycosylated hemoglobin. Fundus photographs were graded for diabetic retinopathy at baseline, and the same photographs were graded later for the diameters of retinal blood vessels. At each examination, a history of cardiovascular disease events since the last examination (and prior to baseline) was obtained. Mortality was monitored yearly. RESULTS: The 20-year age-adjusted cumulative incidences were 18.1% for angina, 14.8% for myocardial infarction, and 5.9% for stroke. Severity of diabetic retinopathy was associated with angina and stroke. Arteriovenous ratio was associated with myocardial infarction. Of 273 deaths, 176 involved heart disease. The severity of retinopathy and arteriovenous ratio was associated with heart disease mortality. Nephropathy was more informative about the cardiovascular end points than were the blood vessel characteristics. CONCLUSIONS: Incidences of cardiovascular disease, including mortality, were common in people with type 1 diabetes during a 20-year interval. Retinal vascular characteristics were associated with these end points, but this association was confounded by nephropathy.

Adolescent↗
PubMed2001

Analysis of retinal and choroidal circulation during central retinal vein occlusion using indocyanine green videoangiography.

OBJECTIVE: To explore the hemodynamic changes and their correlation with clinical presentation during central retinal vein occlusion. MATERIALS AND METHODS: Retrospective, 2-center study. The medical records of 27 patients with central retinal vein occlusion were reviewed. For each patient, the plasma transit in central retinal vessels and in peripapillary choroidal vessels was analyzed using indocyanine green videoangiography. RESULTS: The incidence of alteration in retinal plasma transit, ie, pulsatile filling of arteries and/or veins and increased arteriovenous filling time, was inversely correlated to duration from the onset but not to funduscopic features. Among the 14 patients with less than 1 month's duration of symptoms, 3 developed chronic macular edema, and impairment of arterial flow preceded its onset. Among the 10 patients with opticociliary circulation, choroidal drainage routes were identified in 5 cases, with pulsatile filling in 3. CONCLUSIONS: Early in the course of central retinal vein occlusion, arterial and/or venous flow alterations are present, irrespective of visual acuity, vein dilation, or fundus hemorrhages. These alterations are less frequent in chronic than in recent-onset central retinal vein occlusion. The mechanisms of these alterations remain uncertain but may involve arterial constriction and/or intermittent venous compression. The relationship between these alterations in retinal flow and the secondary onset of macular edema or capillary nonperfusion deserves further investigation.

Adult↗
PubMed1998

Leukocyte trafficking in experimental autoimmune uveitis in vivo.

Leukocyte trafficking from blood into tissue is a fundamental process in immune surveillance and the immune response to stimuli. Experimental autoimmune uveitis (EAU) is an animal model for posterior uveitis and is mediated by T lymphocytes and macrophages that infiltrate the posterior segment of the eye. To analyze leukocyte migration into retinal tissue during the course of EAU, labeled cells were identified in vivo by scanning laser ophthalmoscopy and in retinal flatmounts by confocal microscopy. Adhesion of blood leukocytes to retinal endothelial cells in vivo was significantly raised 48 h before the appearance of clinical disease, and this correlated with the increased expression of CD54 on retinal vessels. Mitogen-activated spleen cells and CD4+ T cells only entered into retinal tissue in animals with clinical disease and not naive recipients. The disease status of the donor animal had no effect on leukocyte trafficking. These results, which identify leukocyte-endothelial cell interactions in vivo, suggest that the activation of the retinal endothelium is a prerequisite to leukocyte adhesion and extravasation into ocular tissue during EAU.

Animals↗
PubMed1995

Coloboma of the optic disk associated with retinal vascular abnormalities.

PURPOSE: We studied a case of congenital optic disk pit and coloboma with associated malformations of the retinal vessels. METHODS: Slit-lamp biomicroscopy and fluorescein angiography were performed. RESULTS: Multiple retinal venous anastomoses associated with a congenital coloboma and pit of the optic disk were observed. The retinal vascular anomalies extended from the optic disk to the temporal periphery. CONCLUSIONS: We consider the coexistence of retinal venous anastomoses with optic disk coloboma and pit to be an extremely rare congenital retinal anomaly.

Abnormalities, Multiple↗
PubMed2002

[The study of immunofluorescence on the retinal digest preparations].

PURPOSE: To study the technique of immunofluorescence staining on the digested retina preparations. METHODS: Retinas of 5 normal Wistar rats and 5 STZ diabetic Wistar rats of were used to make digested retina preparations and carry out immunofluorescence staining with the vascular cell adhesion molecule-1 (VCAM-1). RESULT: The retinal vessels were clearly observed; There were a lot of positive cells in the retinal preparations of the diabetic Wistar rats, while there were no positive cells in the retinal preparations of the normal rats. CONCLUSION: It is feasible to carry out immunofluorescence staining on the digested retina preparations.

Animals↗