Retinal Vasculature (retinal + vasculature)

Distribution by Scientific Domains

Selected Abstracts

Attenuation of retinal vascular development and neovascularization in transgenic mice over-expressing thrombospondin-1 in the lens

Zhifeng Wu
Abstract Thrombospondin-1 (TSP1) is an endogenous inhibitor of angiogenesis and induces endothelial cell (EC) apoptosis. To study the role TSP1 plays during vascular development and neovascularization, we assessed the effects of ectopic TSP1 expression in the lens on retinal vascularization in transgenic mice. The TSP1 over-expressing mice showed abnormalities in the development of retinal vasculature. There was a dramatic decrease in the density of superficial and deep vascular plexuses of the retina in transgenic mice. The retinal vessels in TSP1 transgenic mice also appeared nonuniform and abnormal in maturation. We detected an increase in the number of EC undergoing apoptosis, which was compensated, in part, by an increase in cell proliferation in retinal vasculature of TSP1 transgenic mice. The TSP1 transgenic mice also exhibited increased levels of vessel obliteration and a limited preretinal neovascularization during oxygen-induced ischemic retinopathy (OIR). Our results indicate increased expression of TSP1 attenuates normal retinal vascularization and preretinal neovascularization during OIR. Therefore, modulation of TSP1 expression may provide an effective mechanism for regulation of ocular angiogenesis. Developmental Dynamics 235:1908,1920, 2006. © 2006 Wiley-Liss, Inc. [source]

Retinal vascular image analysis as a potential screening tool for cerebrovascular disease: a rationale based on homology between cerebral and retinal microvasculatures

Niall Patton
Abstract The retinal and cerebral microvasculatures share many morphological and physiological properties. Assessment of the cerebral microvasculature requires highly specialized and expensive techniques. The potential for using non-invasive clinical assessment of the retinal microvasculature as a marker of the state of the cerebrovasculature offers clear advantages, owing to the ease with which the retinal vasculature can be directly visualized in vivo and photographed due to its essential two-dimensional nature. The use of retinal digital image analysis is becoming increasingly common, and offers new techniques to analyse different aspects of retinal vascular topography, including retinal vascular widths, geometrical attributes at vessel bifurcations and vessel tracking. Being predominantly automated and objective, these techniques offer an exciting opportunity to study the potential to identify retinal microvascular abnormalities as markers of cerebrovascular pathology. In this review, we describe the anatomical and physiological homology between the retinal and cerebral microvasculatures. We review the evidence that retinal microvascular changes occur in cerebrovascular disease and review current retinal image analysis tools that may allow us to use different aspects of the retinal microvasculature as potential markers for the state of the cerebral microvasculature. [source]

Roles of Endothelial Cell Migration and Apoptosis in Vascular Remodeling during Development of the Central Nervous System

ABSTRACT Objective: To examine the roles of apoptosis, macrophages, and endothelial cell migration in vascular remodeling during development of the central nervous system. Methods: The terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL) technique was combined with Griffonia simplicifolia isolectin B4 histochemistry to detect apoptotic endothelial cells in retinal whole-mount preparations derived from rats at various stages of postnatal development as well as from rat pups exposed to hyperoxia. Macrophages were detected by immunohistochemistry with the monoclonal antibody ED1, and proliferating endothelial cells were identified by incorporation of bromodeoxyuridine. Results: Only small numbers of TUNEL-positive endothelial cells were detected during normal development of the retinal vasculature, with the apoptotic cell density in the inner plexus peaking during the first postnatal week and decreasing markedly during the second week, at a time when vessel retraction was widespread. Neither apoptotic endothelial cells nor macrophages were apparent at sites of initiation of vessel retraction. TUNEL-positive endothelial cells were observed in vessels destined to remain. Hyperoxia induced excessive vessel withdrawal, resulting in the generation of isolated vascular segments containing apoptotic endothelial cells. A topographical analysis showed low numbers of proliferating endothelial cells at sites of angiogenesis whereas vascular proliferation was increased in the adjacent inner plexus. Conclusions: Endothelial cell apoptosis and macrophages do not initiate vessel retraction, but rather contribute to the removal of redundant cells throughout the vasculature. We suggest that vessel retraction is mediated by endothelial cell migration and that endothelial cells derived from retracting vascular segments are redeployed in the formation of new vessels. Only when retraction results in compromised circulation and redeployment is not possible, does endothelial cell apoptosis occur. [source]

Spatial patterning of cholinergic amacrine cells in the mouse retina

Irene E. Whitney
Abstract The two populations of cholinergic amacrine cells in the inner nuclear layer (INL) and the ganglion cell layer (GCL) differ in their spatial organization in the mouse retina, but the basis for this difference is not understood. The present investigation examined this issue in six strains of mice that differ in their number of cholinergic cells, addressing how the regularity, packing, and spacing of these cells varies as a function of strain, layer, and density. The number of cholinergic cells was lower in the GCL than in the INL in all six strains. The nearest neighbor and Voronoi domain regularity indexes as well as the packing factor were each consistently lower for the GCL. While these regularity indexes and the packing factor were largely stable across variation in density, the effective radius was inversely related to density for both the GCL and INL, being smaller and more variable in the GCL. Consequently, despite the lower densities in the GCL, neighboring cells were more likely to be positioned closer to one another than in the higher-density INL, thereby reducing regularity and packing. This difference in the spatial organization of cholinergic cells may be due to the cells in the GCL having been passively displaced by fascicles of optic axons and an expanding retinal vasculature during development. In support of this interpretation, we show such displacement of cholinergic somata relative to their dendritic stalks and a decline in packing efficiency and regularity during postnatal development that is more severe for the GCL. J. Comp. Neurol. 508:1,12, 2008. © 2008 Wiley-Liss, Inc. [source]

Lens opacity and refractive influences on the measurement of retinal vascular fractal dimension

Haitao Li
Acta Ophthalmol. 2010: 88: e234,e240 Abstract. Purpose:, To examine the influence of lens opacity and refraction on the measurement of retinal vascular fractal dimension (Df). Methods:, Optic disc photographs (right eyes) of 3654 baseline Blue Mountains Eye Study participants (aged 49,97 ) were digitized. Retinal vascular Df was quantified using a computer-based program. Summated severity scores for nuclear, cortical and posterior subcapsular (PSC) cataract were assessed from lens photographs. Refraction data were converted to spherical equivalent refraction (SER), as sum spherical plus 0.5 cylinder power. Axial length was measured at 10-year follow-up examinations using an IOL master. Results:, Mean Df of the retinal vasculature was 1.444 ± 0.023 for 2859 eligible participants. Increasing lens opacity scores were associated with significant reduction in Df (, = ,0.0030, p < 0.0001). Both cortical and PSC cataract involving central lens area were associated with reduced Df, after controlling for confounding factors (ptrend , 0.0105). Increasing myopia severity was associated with reduced Df after adjusting for lens opacity scores and other confounders (ptrend < 0.0001). The slope of Df decrease per SER reduction was 0.0040 in eyes with SER , ,4D, compared to ,0.0016 in eyes with SER > ,4D. For axial length quintiles, there were no significant differences in mean Df in all groups except a reduction in the fifth quintile (axial length ,24.15 mm) (all p < 0.05). Conclusion:, Ocular media opacity independently influenced retinal vascular Df measurement, but we found no evidence supporting any refractive axial magnification effect on this measure. Myopic refraction ,,4D was associated with a reduction in Df, suggesting rarefaction of retinal vasculature associated with high myopia. [source]

3254: Neurovascular coupling in the retrobulbar ciliary circulation

Purpose Perfusion of the retina is adapted to the metabolic demand by neurovascular coupling. Neurovascular coupling has shown to be present in the retinal vasculature, but not in vessels supplying the optic nerve. The present study investigated the presence of neurovascular coupling in the anterior part of the optic nerve in healthy and glaucoma subjects. Methods Retrobulbar blood flow velocities were determined by color Doppler imaging (CDI). A Siemens Elegra ultrasound system with a 7.5L40 transducer was used. Peak-systolic and end-diastolic velocities (PSV and EDV) in the central retinal artery (CRA) or the short posterior ciliary artery (SPCA) were the primary readout. CDI measurements were performed shortly before, during, immediately after, 60 s after, and 120 s after a 10-Hz flicker stimulation of the retina. Results Thirty-five glaucoma patients and 44 healthy control subjects were included in the study. In the SPCA of healthy controls, flicker stimulation led to a rise of PSV from 9.7±0.8 to 12.5±0.8 cm/s (P<0.001; N=24) and of EDV from 2.4±0.3 to 3.6±0.3 cm/s (P<0.001; N=24). This effect was not detectable in glaucoma patients. In the CRA, flicker light led to an increase of EDV from 2.1±0.2 to 3.0±0.3 cm/s (P=0.002; N=20) in healthy volunteers and from 1.3±0.2 to 2.0±0.2 cm/s in glaucoma patients (P=0.004; N=15). PSV was affected by flicker stimulation in neither the healthy volunteers nor glaucoma patients. Conclusion The data indicate the presence of neurovascular coupling in the vascular bed supplied by the paraoptic SPCA. The response pattern to the flicker stimulus differs between healthy and glaucoma subjects. [source]

4145: Analysis of mouse eye mutants as models for human diseases

Purpose The Eumodic (European Mouse Disease Clinic) project screens mouse knockout lines and ENU induced mutants for pathological phenotypes. Initially 2 of the strains identified with an eye defect by the Sanger MGP and a strain from the ENU mutagenesis screen at MRC Harwell have been selected for further investigation. Methods Following the initial primary phenotyping, pathology; histology; and immunohistochemistry was carried out on ocular tissue collected from mutant and control animals to determine defects in eye structure and development. This gave an indication to the underlying cause of the defects seen, enabling further molecular biology analysis. Results Btb/Poz Domain-containing Protein 12 (Btbd12) is a scaffold protein required for the formation of DNA repair complexes. The mouse knockout of this gene shows corneal opacity, dilated pupils and occasional microphthalmia, modelling the phenotypes seen in human diseases of defective DNA repair. The corneas of the mutant animals exhibit increased DNA damage which is likely to be the cause of the opacification. Solute Carrier Family 9 Member 8 (Slc9a8) is a Sodium/ Hydrogen exchanger and has previously been shown to play a role in ion exchange. The Slc9a8 knockout strain appears to have retinal degeneration and the males are infertile. The ENU-induced mutant Pedv128 exhibits defects in the retinal vasculature including defective vascular patterning and increased vascular leakage. Of particular interest is that this vascular phenotype is restricted to the eyes. Conclusion Investigation of mouse eye mutants can result in a better understanding of the pathology and underlying causes of human diseases. [source]

Longterm follow-up of children with traumatic optic nerve avulsion

Veit Sturm
Abstract. Purpose:, We report the longterm follow-up of children with optic nerve avulsion (ONA) caused by traumatic events. The remarkable differences in courses and outcomes may elucidate the spectrum of ONA-associated symptoms and injuries. Methods:, During the last 15 years, three children with ONA were referred to our department. These cases are presented with special attention to their longterm follow-up. Results:, Two patients suffered from complete ONA after head injury. The third patient presented with partial ONA caused by a bicycle accident. Longterm follow-up varied between 7 and 15 years. In the first patient, a pale swollen retina without any visible retinal vasculature was observed early in the course of follow-up. The retina later completely detached. In the second patient, extended fibroglial scarring occurred and an extremely large epiretinal membrane formed and was finally released spontaneously into the vitreous. The third patient developed only mild fibroglial scarring and retinal pigment epithelium hyperplasia. The optic nerve head in this patient came to resemble a morning glory disc. Conclusions:, Optic nerve avulsion can adopt different courses and outcomes in different patients. Final visual outcome seems to depend on the degree of visual acuity immediately after injury. Substantial intraocular architecture changes can occur as a result of ONA. [source]

Ocular blood flow and oxygen delivery to the retina in primary open-angle glaucoma patients: the addition of dorzolamide to timolol monotherapy

Brent Siesky
Abstract Purpose:, To assess the effects of adding dorzolamide to timolol monotherapy on ocular haemodynamics and retinal oxygen saturation in patients with primary open-angle glaucoma (POAG). Methods:, Twenty-four patients (12 healthy, 12 with POAG) were treated with dorzolamide/timolol combination (DT) versus timolol maleate 0.5% twice daily in a randomized, crossover, double-blind study conducted over a period of 18 months. Patients received each treatment for 8 months then crossed over to the other treatment after a 1-month washout and second baseline. Goldmann applanation tonometry, Heidelberg retinal flowmetry (HRF), colour Doppler imaging (CDI) and retinal photographic oximetry were performed at each visit. Results:, DT significantly reduced intraocular pressure (IOP) in both glaucomatous [right eye (OD) ,13.15%, left eye (OS) ,14.43%; p < 0.036] and non-glaucomatous (OD ,12.4%, OS ,13.88%; p < 0.039) patients compared to timolol after 8 months of treatment. DT significantly reduced the number of zero blood flow pixels in the superior (,39.72%; p < 0.014) and inferior (,51.44%; p < 0.008) retina in the non-glaucomatous group and inferior retina in the glaucomatous group (,55.38%, p < 0.006). The continuation of timolol monotherapy from baseline did not change (p < 0.05) any measured parameter and neither treatment had a significant effect (p < 0.05) on retinal oximetry or CDI parameters. Conclusion:, The addition of dorzolamide to timolol monotherapy decreases IOP and increases retinal blood flow in the superficial retinal vasculature in both glaucomatous and healthy patients following 8 months of treatment. The combination of increased retinal blood flow with consistent oxygen saturation may potentially increase oxygen delivery to the retina. [source]

Microstructural alterations of the retinal arterial blood column along the vessel axis in healthy volunteers with age

Purpose We demonstrated previously that roughness of the retinal arterial blood column measured along the vessel axis increases in anamnestically healthy volunteers with increasing age. We termed it longitudinal retinal arterial profile (LAP). Whether LAP is altered with age in medically supervised healthy persons is investigated. Methods 82 medically healthy volunteers were examined by Dynamic Vessel Analyzer (IMEDOS, Jena, Germany) using stimulation with flickering light. 3 age groups were formed: young (N=27, 30,5±4,3 years), middle age (N=28, 42,3±3,3 years) and seniors (N=27, 64,0±5,0 years). Included in the analysis were volunteers without medical vascular risk factors defined as: blood pressure < 140/90 mmHg, HDL > 35 mg/dl, LDL < 190 mg/dl and glucose levels < 110 mg/dl. Retinal arterial diameters were measured along 1 mm vessel segments to obtain LAP. Differences were analyzed using Fourier transformation. Results In all age groups LAP do not change during all stages of the arterial response. Arterial diameters in the senior group were reduced in comparison to the young group at all stages of the vessel reaction (p<0,05). There are differences in LAP between the age groups. Compared to young persons, seniors showed significantly diminished waves with a period of 417 µm at all stages of the arterial reaction, whereas young volunteers showed less pronounced waves with a period of 208 µm (p<0,05). Conclusion Our results represent the healthy aging process in retinal vasculature. Age related microstructural changes in longitudinal profiles of retinal arteries in medically healthy persons might be an indication for alterations in the vascular endothelium and smooth musculature. [source]

New insights into the development of retinopathy of prematurity , importance of early weight gain

A Hellström
Abstract Evidence is accumulating that one of the strongest predictors of retinopathy of prematurity (ROP), in addition to low gestational age, is poor weight gain during the first weeks of life. In infants born preterm, the retina is not fully vascularised. The more premature the child, the larger is the avascular area. In response to hypoxia, vascular endothelial growth factor (VEGF) is secreted. For appropriate VEGF-induced vessel growth, sufficient levels of insulin-like growth factor I (IGF-I) in serum are necessary. IGF-I is a peptide, related to nutrition supply, which is essential for both pre- and post-natal general growth as well as for growth of the retinal vasculature. In prematurely born infants, serum levels are closely related to gestational age and are lower in more prematurely born infants. At preterm birth the placental supply of nutrients is lost, growth factors are suddenly reduced and general as well as vascular growth slows down or ceases. In addition, the relative hyperoxia of the extra-uterine milieu, together with supplemental oxygen, causes a regression of already developed retinal vessels. Postnatal growth retardation is a major problem in very preterm infants. Both poor early weight gain and low serum levels of IGF-I during the first weeks/months of life have been found to be correlated with severity of ROP. Conclusion: This review will focus on the mechanisms leading to ROP by exploring factors responsible for poor early weight gain and abnormal vascularisation of the eye of the preterm infant. [source]