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Results for “Retinal Neovascularization”

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At least 775 records · Page 43Linked to original sources
PubMed1989

Morphologic observations of retinal pigment epithelial proliferation and neovascularization in the rabbit.

Neovascularization and proliferation of the retinal pigment epithelium (RPE) was induced in the rabbit by subretinal injection of vitreous without rupture of Bruch's membrane. New vessels developed between the layer of RPE and photoreceptor outer segments, but were enveloped in proliferating RPE. For this reason they were occult; no fluorescein leakage was visible by angiography. The vessels were identified only by histologic examinations. Endothelial cell budding was the initial stage of vessel development, first seen two weeks after injection. The new vessels grew from the choriocapillaris, penetrated Bruch's membrane, and spread into the subretinal space, despite the absence of subretinal fluid. Fenestrations with diaphragms were found in the endothelial walls during the earliest stages of vessel formation, and were also present in the fully matured vessels. Intermediate junctional complexes were frequently observed among the endothelial cells. During maturation of these plexi, junctions changed from open to putative tight junctions. The mature vessels were ultimately completely enveloped by collagen and RPE cells. Our results show that all new vessels in this animal model have the morphologic characteristics of choriocapillaris. We assume that they leak fluorescein, as does the choriocapillaris, but that the dye has no opportunity to pool in the subretinal space and thus cannot be seen during angiography.

Animals↗
PubMed2003

Periocular gene transfer of sFlt-1 suppresses ocular neovascularization and vascular endothelial growth factor-induced breakdown of the blood-retinal barrier.

Vascular endothelial growth factor (VEGF) is a critical stimulus for both retinal and choroidal neovascularization, and for diabetic macular edema. We used mouse models for these diseases to explore the potential of gene transfer of soluble VEGF receptor-1 (sFlt-1) as a treatment. Intravitreous or periocular injection of an adenoviral vector encoding sFlt-1 (AdsFlt-1.10) markedly suppressed choroidal neovascularization at rupture sites in Bruch's membrane. Periocular injection of AdsFlt-1.10 also caused significant reduction in VEGF-induced breakdown of the blood-retinal barrier, but failed to significantly inhibit ischemia-induced retinal neovascularization. Periocular delivery of an adenoviral vector encoding pigment epithelium-derived factor (PEDF), another secreted protein, resulted in high levels of PEDF in the retinal pigmented epithelium and choroid, but not in the retina. This may explain why periocular injection of AdsFlt-1.10 inhibited choroidal, but not retinal neovascularization. Periocular delivery offers potential advantages over other routes of delivery and the demonstration that sFlt-1 enters the eye from the periocular space in sufficient levels to achieve efficacy in treating choroidal neovascularization and retinal vascular permeability is a novel finding that has important clinical implications. These data suggest that periocular gene transfer of sFlt-1 should be considered for treatment of choroidal neovascularization and diabetic macular edema.

Adenoviridae↗
PubMed1997

Indocyanine green angiography-guided photocoagulation of choroidal neovascularization associated with retinal pigment epithelial detachment.

PURPOSE: To determine visual acuity outcome after indocyanine green angiography-guided laser photocoagulation of choroidal neovascularization associated with pigment epithelial detachment in eyes with age-related macular degeneration. METHODS: We retrospectively reviewed pretreatment and posttreatment visual acuity after laser photocoagulation to well-demarcated hyperfluorescent areas seen with indocyanine green angiography adjacent to or within pigment epithelial detachments in 20 eyes of 20 patients with age-related macular degeneration and suspected choroidal neovascularization. RESULTS: Visual acuity before and after laser photocoagulation was followed up for 3 to 24 months (median, 9 months). At 3 months after laser photocoagulation, visual acuity had improved 2 or more Snellen lines in two eyes (10%), worsened by 2 or more lines in 10 (50%), and remained unchanged in eight of 20 (40%). By 6 months after laser photocoagulation, visual acuity had improved by 2 or more lines in two eyes (12%), worsened by 2 or more lines in nine (53%), and remained unchanged in six of 17 (35%). At 9 months after laser photocoagulation, visual acuity had improved by 2 or more lines in one eye (9%), worsened by 2 or more lines in nine (82%), and remained unchanged in one of 11 (9%). CONCLUSIONS: Indocyanine green angiography-guided laser photocoagulation may temporarily stabilize visual acuity in some eyes with choroidal neovascularization associated with pigment epithelial detachments, but final visual acuity decreases with time.

Aged↗
PubMed1987

Dominant macular subretinal neovascularization with peripheral retinal degeneration.

A previously undescribed dominant macular dystrophy was found in five individuals from a four-generation pedigree. According to family history, three additional individuals were similarly affected. The disease was characterized by loss of central vision from macular subretinal neovascularization in the third to fourth decade. Four of these individuals complained of nyctalopia beginning in childhood. All five were myopic. Funduscopic findings in the posterior pole included subretinal neovascular membranes and yellow punctate deposits appearing at the level of the retinal pigment epithelium (RPE). Mid-peripheral and equatorial retinal pigment clumping and pigment migration were also observed. Abnormalities of electrophysiologic testing were suggestive of an early retinal degeneration.

Adolescent↗
PubMed2000

Sensitivity of different vascular beds in the eye to neovascularization and blood-retinal barrier breakdown in VEGF transgenic mice.

Neovascularization (NV) causes visual deficits in ocular disorders such as diabetic retinopathy, age-related macular degeneration, and retinopathy of prematurity. An understanding of the angiogenic factors promoting this abnormal vascular growth is necessary to devise a therapeutic approach to inhibit NV. One factor known to promote NV is vascular endothelial growth factor (VEGF), which can also induce a breakdown of the blood-retinal barrier (BRB) leading to macular edema, another major cause of visual loss in a variety of ocular disorders. To investigate the role of VEGF on ocular NV, transgenic mice have been produced that over-express VEGF in the photoreceptors under control of the rhodopsin promoter. Eyes from these mice and from littermates not expressing the transgene were examined using immunohistochemistry, griffonia simplicifolia isolectin-B4 (GSA) staining to clearly visualize vessels, and electron microscopy. Levels of transgene expression were determined by the polymerase chain reaction. In normal mice, retinal vessels are organized into a superficial and a deep capillary bed with some vessels forming a shunt between both beds. In a transgenic line of mice that over-expresses VEGF (V-6), NV originates from the deep capillary bed at about postnatal day 10 (P10) and extends through the photoreceptor layer to form vascular complexes in the subretinal space with BRB breakdown occurring only in the area of NV. The superficial capillary bed and the choroidal vasculature are unaffected. In another line of transgenic mice with a higher expression rate of VEGF (V-24), photoreceptor degeneration begins at P7-8, soon after the onset of transgene expression, without widespread NV, as was observed in V-6 mice. In conclusion, overexpression of VEGF in transgenic mice is sufficient to cause retinal NV, but only the deep capillary bed is responsive. Increasing the expression of VEGF does not necessarily increase the amount of NV. A better understanding of the specific factors and conditions that result in a particular pattern of ocular NV may provide clues regarding the pathogenesis of ocular neovascular disease.

Animals↗
PubMedDate not supplied

Branch retinal artery occlusion (BRAO) combined with branch retinal vein occlusion (BRVO) and optic disc neovascularization associated with HIV and CMV retinitis.

Two vaso-occlusive events, branch retinal artery occlusion (BRAO) and branch retinal vein occlusion (BRVO), were observed in the retina of an HIV-infected patient with cytomegalovirus (CMV) retinitis who developed neovascularization of the disc (NVD). Although BRVO and reversible NVD have been reported in association with CMV retinitis, we have seen no reports of concomitant BRAO. CMV damages endothelial cells and causes an occlusive vasculitis. In HIV-infected individuals, damaged endothelial cells and rheologic problems result in increased blood viscosity. HIV infection has also been associated systemically with elevated levels of cytokines, including tumor necrosis factor alpha (TNF-alpha). In vitro, TNF-alpha exerts effects that decrease fibrinolytic potential; this activity in the circulation of a patient with AIDS may lead to vascular occlusive events. In the patient reported here, the retinal changes were not reversed by induction therapy with ganciclovir and the NVD did not regress.

AIDS-Related Opportunistic Infections↗
PubMed1976

Senile mecular degeneration. A clinicopathologic correlation of two cases with neovascularization beneath the retinal pigment epithelium.

The histopathologic findings in two cases of senile macular degeneration were correlated with the premortem clinical studies, from the onset in both cases and through the disciform stage in one case. In case 2, the postmortem eyes were obtained only one month after ophthalmoscopic, fluorescein angiographic, and fundus photographic studies were performed, all on the same day. Our report not only adds to the few clinicopathologic correlations of the lesions in senile macular degeneration reported in the literature, but also presents the first reconstruction to scale of subretinal pigment epithelial (sub-RPE) neovascularization. Our results confirm the diagnosis of sub-RPE neovascularization and serous detachment of the retinal pigment epithelium. Drusen were correlated as to number and general location but not individually. Serous detachment of the neurosensory retina was found histopathologically but not clinically.

Aged↗
PubMed1990

Profound central visual loss and ocular neovascularization in idiopathic recurrent branch retinal arterial occlusion.

The authors report a 65-year-old healthy, white man who experienced a dramatic loss of central vision. Iris neovascularization, rubeotic glaucoma, disc neovascularization and subhyaloid hemorrhage developed after multiple, recurrent, idiopathic branch retinal arterial occlusions. Vitreous and perivascular inflammation were prominent associated clinical features. Systemic steroids were useful in suppressing intraocular and perivascular inflammation, yet neither steroid nor anticoagulant therapy effectively prevented recurrent occlusive episodes. Retinal neovascularization and rubeotic glaucoma were successfully managed with scatter panretinal photocoagulation. Episodic intraocular inflammation and ocular neovascularization have been noted in one-third of patients sustaining recurrent idiopathic branch retinal arterial occlusions.

Aged↗
PubMed1994

[Neovascularization in experimental retinal venous obstruction in rabbit].

Experimental retinal venous obstruction was produced in rabbit eyes by transadventitial instillation of thrombin for the purpose of studying the late stage of histopathological changes in the retina. Three months after the instillation, abnormal vessels and compensatory shunt vessels were observed by ophthalmoscopy. Capillary obstruction, blood leakage from venules and neovascularization were observed on gelatin-fluorescein injected flat preparations of the retina three months after the thrombus formation. Although venular lumina were first narrowed and restored to normal three months after thrombin instillation, the lumina of arterioles remained narrow and intraluminal fibrin thrombi were present in the arterioles more than three months later in light microscopy. In electron microscopy many ribosomes and large nuclei were observed in newly formed retinal vessels, and their basement membranes were thin and discontinuous. Ghost vessels penetrated by glial cell processes were also found in the proliferative tissues. These results suggest that neovascularization occurs when the intraretinal damages last more than 3 months after the onset of thrombogenesis.

Animals↗
PubMed2001

Retinal ischemia and angle neovascularization in proliferative diabetic retinopathy.

PURPOSE: To analyze the relationship between the extent of retinal ischemia in proliferative diabetic retinopathy and angle neovascularization. METHODS: Panoramic fundus fluorescein angiography and 360-degree fluorescein gonioangiography to detect the angle neovascularization were performed on 70 eyes of 46 patients with proliferative diabetic retinopathy. Statistical significance was evaluated by chi-squared test. Statistical significance was evaluated if the value (T) was greater than the level of significance, chi(0.05)(2)(2) = 5.99. RESULTS: Retinal ischemia in fluorescein angiography was evaluated in four areas: capillary occlusion in (1) temporal raphe; (2) radial peripapillary capillaries; (3) the midperiphery (grade I, less than 25% of the area; grade II, 25% to 50%; grade III, 50% to 75%; grade IV, more than 75%); and (4) optic disk with neovascularization. The angle neovascularization was divided into two types: type I (14 eyes) and type II (12 eyes). Capillary occlusion in the temporal raphe and radial peripapillary capillaries, and papillary leakage significantly increased the risk of angle neovascularization (T = 8.28, 10.04, 6.44 respectively). Grade III and IV capillary occlusion in the midperiphery had a significant risk of angle neovascularization when compared with grade I (between grade III: T = 9.03, grade IV: T = 19.36) and II (between grade III: T = 6.31, grade IV: T = 16.09). CONCLUSION: Risk factors for angle neovascularization were retinal nonperfusion in the midperiphery wider than grade III, capillary occlusion in the radial peripapillary capillaries and temporal raphe, and optic disk. Fluorescein gonio angiography was found to be a powerful tool for the early detection of angle neovascularization, especially in dark irides.

Adult↗
PubMed1996

Rod photoreceptor transduction is affected in central retinal vein occlusion associated with iris neovascularization.

Patients with central retinal vein occlusion who later develop iris neovascularization show changes in the amplitude, the timing, and the sensitivity of the electroretinogram beta wave. We determined the extent to which rod photoreceptor dysfunction contributes to these changes by recording single-flash electroretinograms from both eyes of 52 patients with unilateral central retinal vein occlusion and fitting the leading edges of alpha waves with a model of rod phototransduction. Eyes with central retinal vein occlusion showed reductions in photoreceptor gain but no changes in photoreceptor amplitude when compared with the fellow eyes. The reductions were larger in eyes that developed iris neovascularization and were predictive of this complication. Photoreceptor gain reductions accounted for only part of the beta-wave timing delays and sensitive loss; the remainder is attributed to functional loss in the inner nuclear layer.

Adult↗