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PubMed1996

The effect of postnatal growth retardation on abnormal neovascularization in the oxygen exposed neonatal rat.

Severe retinopathy of prematurity (ROP) occurs in the smallest and sickest of premature infants. We hypothesized that, in a rat model of oxygen induced retinopathy, abnormal neovascularization would occur more frequently in larger litters where the pups are subject to postnatal growth retardation. Four litters of newborn Sprague-Dawley rats were studied; rats were randomly mixed to form two large litters (n = 25 each) and two small litters (n = 10 each). All litters were exposed to 7 days cyclic hyperoxia and hypoxia followed by 5 days in room air. ADPase stained retinae were evaluated in a masked manner for the presence and severity of abnormal neovascularization. Fluorescein perfused retinae were digitized and the ratios of vascularized:total retinal area were calculated using computer assisted image analysis. As expected, final weight in the large litters was less than in the small litters (15.3 +/- 3.8g vs. 23.4 +/- 2.1g, p < 0.001). Neovascularization occurred in 53% of rats in the large litters vs. 15% in the small litters (p = 0.009). Rats with retinae demonstrating neovascularization were smaller than those without (16.2 +/- 4.7g vs. 19.6 +/- 5.0g, p = 0.016). The severity of neovascularization in clock h was inversely correlated with final weight (rs = -0.35, p = 0.01) and ratio of vascularized:total retina area (rs = -0.46, p < 0.001). Smaller rat pups raised in larger litters, with resultant growth retardation, develop more frequent and more severe abnormal retinal neovascularization. Our results correlate with clinical experience in the premature infant.

Animals↗
PubMed1995

[Indocyanine green angiography in retinal hemorrhage of uncertain origin].

BACKGROUND: With the development of new imaging technologies indocyanine green (ICG) angiography allows better visualization of choroidal and retinal vasculature and their pathology. Due to its high protein bound ICG leaks very slowly from fenestrated normal and abnormal vessels. With its absorption and emission peak in the near infrared spectrum ICG penetrates hemorrhage to a greater degree than does blue light with shorter wavelength used for fluorescein angiography. METHODS: We report the clinical and fluoresceinangiographical findings of three patients with a sudden macular hemorrhage of unknown origin. RESULTS: In all patients conventional fluoresceinangiography revealed a similar appearance with little characteristic signs early ill-defined hyperfluoroescence and late exudation of dye. ICG angiography clearly demonstrated the underlying pathology as a pulsatile retinal artery macroaneurysm, a choroidal neovascularization secondary to age-related macular degeneration, and a retinal angioma. CONCLUSION: ICG videoangiography with its absorption and emission peak in the near infrared light seems to be an additive tool to identify and delineate more precisely fluoresceinangiographically ill-defined hyperfluorescence and exudations in patients with retinal hemorrhage of unknown origin.

Aged↗
PubMedDate not supplied

The effect of L-thyroxine supplementation in a neonatal rat model of ROP.

PURPOSE: The role of L-thyroxine in retinopathy of prematurity (ROP) is controversial. Recent animal studies suggest both high and low levels of serum thyroxine (exogenous supplementation and pharmacologic inhibition) are associated with preretinal neovascularization (NV) or retinal vascular retardation, a precursor of NV. To address this controversy, we studied L-thyroxine supplementation in an animal model of ROP. METHODS: Five hundred newborn Sprague-Dawley rats were raised in 20 expanded litters of 25, under conditions of fluctuating high and low oxygen and high carbon dioxide, to induce preretinal neovascularization. Rats received either 3 days of intraperitoneal T4, 7 days of T4 or saline control. Doses of T4 ranged from 0.005 microg/g to 0.5 microg/g. Retinae from left eyes were dissected, flat-mounted, and ADPase-stained. The presence and severity of NV, retinal vascular area, and retinal vascular density were scored in a masked manner. RESULTS: The incidence of NV was similar in rats receiving either 3 days of T4 or 7 days of T4 and saline controls (55% and 43% NV in 3-day experiments [0.05 microg g-1 day-1 and 0.5 microg g-1 day-1] compared with 51% in saline controls, p = 0.49; 52% and 38% in 7-day experiments [0.005 microg g-1 day-1 and 0.05 microg g-1 day-1], p = 0.22). Retinal vascular area and vessel density were also similar to saline controls. CONCLUSIONS: Systemic T4 supplementation does not increase, or decrease, the incidence or severity of preretinal neovascularization in an animal model of ROP, despite its positive effect on overall animal growth. Further work is needed to elucidate the potential role of premature infant hypothyroidism in the pathogenesis of ROP.

Animal Nutritional Physiological Phenomena↗
PubMed1996

Identification and characterization of vascular endothelial growth factor receptor (Flt) in bovine retinal pericytes.

Vascular endothelial growth factor (VEGF) plays an important role in the hypoxia-stimulated neovascularization of ischemic retinal diseases such as proliferative diabetic retinopathy. VEGF exerts its effect through two known high-affinity tyrosine kinase receptors, named kinase insert domain-containing receptor (KDR) and the fms-like tyrosine kinase (Flt). VEGF receptors are located primarily on endothelial cells, although receptors on a few other nonocular cell types also have been described. In the present study, we demonstrate the expression of Flt, but not KDR, in bovine retinal pericytes (BRPCs). Although KDR is expressed predominantly in retinal endothelial cells, Northern blot analysis demonstrated substantial expression of the Flt gene in BRPCs without detection of KDR despite using polyadenylated RNA. Hypoxia increased Flt gene expression in BRPCs (2.7-fold, P < 0.01). 125I-labeled VEGF binding analysis on BRPCs demonstrated two apparent high-affinity receptor subtypes (Kd = 14 and 215 pmol/l), with 2.9 x 10(4) and 1.4 x 10(5) receptors/cell, respectively. 125I-VEGF affinity cross-linking demonstrated VEGF-specific binding complexes at 150, 172, 187, and 200 kDa under reducing conditions. Western blot analysis using an anti-phosphotyrosine antibody demonstrated VEGF-induced tyrosine phosphorylation of several proteins. VEGF stimulation had little effect on initial BRPCs growth rates but significantly increased BRPCs number after 7 days. These results suggest that two classes of high-affinity VEGF receptors are present on BRPCs, at least one of which is analogous to Flt and is capable of intracellular protein phosphorylation. Thus, VEGF might regulate the function of both retinal endothelial cells and retinal pericytes to induce pathological angiogenesis and vascular remodeling during proliferative diabetic retinopathy and other ischemic retinal diseases.

Animals↗
PubMed2005

Inhibition of tumor necrosis factor-alpha improves physiological angiogenesis and reduces pathological neovascularization in ischemic retinopathy.

The present study was undertaken to test whether inhibition of the proangiogenic inflammatory cytokine tumor necrosis factor (TNF)-alpha can modulate retinal hypoxia and preretinal neovascularization in a murine model of oxygen-induced retinopathy (OIR). OIR was produced in TNF-alpha-/- and wild-type (WT) control C57B6 neonatal mice by exposure to 75% oxygen between postnatal days 7 and 12 (P7 to P12). Half of each WT litter was treated with the cytokine inhibitor semapimod (formerly known as CNI-1493) (5 mg/kg) by daily intraperitoneal injection from the time of reintroduction to room air at P12 until P17. The extent of preretinal neovascularization and intraretinal revascularization was quantified by image analysis of retinal flat-mounts and retinal hypoxia correlated with vascularization by immunofluorescent localization of the hypoxia-sensitive drug pimonidazole (hypoxyprobe, HP). HP adducts were also characterized by Western analysis and quantified by competitive enzyme-linked immunosorbent assay. TNF-alpha-/- and WT mice showed a similar sensitivity to hyperoxia-induced retinal ischemia at P12. At P13 some delay in early reperfusion was evident in TNF-alpha-/- and WT mice treated with semapimod. However, at P17 both these groups had significantly better vascular recovery with less ischemic/hypoxic retina and preretinal neovascularization compared to untreated retinopathy in WT mice. Immunohistochemistry showed deposition of HP in the avascular inner retina but not in areas underlying preretinal neovascularization, indicating that such aberrant vasculature can reduce retinal hypoxia. Inhibition of TNF-alpha significantly improves vascular recovery within ischemic tissue and reduces pathological neovascularization in OIR. HP provides a useful tool for mapping and quantifying tissue hypoxia in experimental ischemic retinopathy.

Animals↗
PubMedDate not supplied

Intrachoroidal dye leakage in indocyanine green fundus angiography after experimental commotio retinae.

Dye leakage in sodium fluorescein (FLUO) fundus angiography indicates damage to the blood-retinal barrier. However, dye leakage in indocyanine green (ICG) fundus angiography does not mean the same, because of the larger molecular size of the dye and impermeability of the choroidal vessels to it. The possibility of dye leakage in ICG angiography has not yet been revealed in an experimental study in which the blood-retinal barrier is undamaged. We report here that intrachoroidal dye leakage may occur in ICG angiography in an experimental model of the traumatic retinal opacity of the rabbit eye, even when the blood-retinal barrier is undamaged. This mechanism of dye leakage in ICG angiography is quite different from the leakage of FLUO angiography. Pathological choroidal vessels with increased permeability, such as choroidal neovascularization under the retinal pigment epithelium, can be observed using ICG angiography.

Animals↗
PubMed2000

Retinal vascular changes associated with transpupillary thermotherapy for choroidal melanomas.

PURPOSE: To define retinal vascular changes after transpupillary thermotherapy (TTT) for choroidal melanomas and assess their clinical impact. METHODS: Stereoscopic fluorescein angiogram pairs of 29 patients pre- and post-treatment with TTT were examined for patterns of vascular damage, and the patients were studied for ensuing complications. RESULTS: Widespread retinal capillary loss was confined within the treatment margins except in cases of coexisting large retinal artery or vein occlusions. Artery occlusions occurred in 83%, involving a large artery in 23%. Venous occlusions occurred in 69%, involving large veins in 10%. Subretinal choroidal neovascularization occurred in four cases, in one causing hemorrhage that broke through into the vitreous. No retinal neovascularization occurred. Choroidal vasculature was relatively preserved at the periphery of the treated area. Foveal vascular damage caused visual loss in six cases. Vascular changes beyond the treatment margins did not affect the fovea in any case. Retinal fibrosis affected two cases. Diabetic patients fared no worse than healthy counterparts. CONCLUSIONS: Transpupillary thermotherapy produces characteristic retinal vascular changes that may reduce vision when affecting the fovea. Vascular changes are confined within the treatment margins except in cases of associated large vessel occlusion. There is a small risk of neovascularization, both retinal and choroidal.

Adult↗
PubMed1994

Vascular endothelial growth factor in ocular fluid of patients with diabetic retinopathy and other retinal disorders.

BACKGROUND: Retinal ischemia induces intraocular neovascularization, which often leads to glaucoma, vitreous hemorrhage, and retinal detachment, presumably by stimulating the release of angiogenic molecules. Vascular endothelial growth factor (VEGF) is an endothelial-cell-specific angiogenic factor whose production is increased by hypoxia. METHODS: We measured the concentration of VEGF in 210 specimens of ocular fluid obtained from 164 patients undergoing intraocular surgery, using both radioimmuno-assays and radioreceptor assays. Vitreous proliferative potential was measured with in vitro assays of the growth of retinal endothelial cells and with VEGF-neutralizing antibody. RESULTS: VEGF was detected in 69 of 136 ocular-fluid samples from patients with diabetic retinopathy, 29 of 38 samples from patients with neovascularization of the iris, and 3 of 4 samples from patients with ischemic occlusion of the central retinal vein, as compared with 2 of 31 samples from patients with no neovascular disorders (P < 0.001, P < 0.001, and P = 0.006, respectively). The mean (+/- SD) VEGF concentration in 70 samples of ocular fluid from patients with active proliferative diabetic retinopathy (3.6 +/- 6.3 ng per milliliter) was higher than that in 25 samples from patients with nonproliferative diabetic retinopathy (0.1 +/- 0.1 ng per milliliter, P = 0.008), 41 samples from patients with quiescent proliferative diabetic retinopathy (0.2 +/- 0.6 ng per milliliter, P < 0.001), or 31 samples from nondiabetic patients (0.1 +/- 0.2 ng per milliliter, P = 0.003). Concentrations of VEGF in vitreous fluid (8.8 +/- 9.9 ng per milliliter) were higher than those in aqueous fluid (5.6 +/- 8.6 ng per milliliter, P = 0.033) in all 10 pairs of samples obtained simultaneously from the same patient; VEGF concentrations in vitreous fluid declined after successful laser photocoagulation. VEGF stimulated the growth of retinal endothelial cells in vitro, as did vitreous fluid containing measurable VEGF. Stimulation was inhibited by VEGF-neutralizing antibodies. CONCLUSIONS: Our data suggest that VEGF plays a major part in mediating active intraocular neovascularization in patients with ischemic retinal diseases, such as diabetic retinopathy and retinal-vein occlusion.

Adolescent↗
PubMed2001

Increased prevalence of microthromboses in retinal capillaries of diabetic individuals.

In diabetic retinopathy, capillary nonperfusion and eventual obliteration can lead to retinal ischemia and sight-threatening neovascularization. The occurrence of retinal microthrombosis in human diabetes has long been suspected and occasionally observed but never systematically demonstrated. We used trypsin digestion to isolate the intact vascular network from retinas obtained postmortem from nine diabetic donors (age 64 +/- 11 years, duration of diabetes 6 +/- 4 years; mean +/- SD) and eight age-matched nondiabetic donors. Topographically matched sectors (each one-sixth of retina) of diabetic and nondiabetic retinas were tested sequentially with antibodies to fibrin cross-linking factor XIII and platelet glycoprotein (GP)-IIIa to identify fibrin-platelet thrombi. In some trypsin digests, we also examined vascular cell apoptosis. The retina from a nondiabetic donor, 24 years of age, who had died of trauma, was used to exclude confounding influences caused by the postmortem period. When compared with those of nondiabetic donors, the retinas of diabetic donors showed double the number of capillary segments with colocalized immunostaining for factor XIII and GPIIIa (P = 0.02). The total area of the positive segments was fourfold greater in the diabetic than in the nondiabetic donors (P = 0.02) and correlated with the duration of diabetes (r = 0.71, P < 0.05). Large thrombi were six times more frequent in the diabetic donors (P = 0.03), and there was a significant topographical association of microthrombosis with apoptotic cells in both diabetic and nondiabetic vessels (P = 0.0001). Hence, diabetes of short duration was found to be associated with a greater than normal number and size of platelet-fibrin thrombi in the retinal capillaries. These thrombi can contribute to capillary obliteration and retinal ischemia and may be a practical target for early drug intervention.

Adult↗
PubMed2002

Angiographic and flow patterns of retinal choroidal anastomoses in age-related macular degeneration with occult choroidal neovascularization.

OBJECTIVE: To identify the angiographic features of retinal choroidal anastomoses (RCAs) in patients with newly diagnosed occult choroidal neovascularization (CNV) in the setting of age-related macular degeneration (AMD) and to determine the sequence of flow between the RCA and the CNV. DESIGN: Retrospective cross-sectional study. PARTICIPANTS: The angiograms of 205 eyes of 153 consecutive patients with occult CNV on fluorescein angiography (FA) and focal hot spots on indocyanine green angiography (ICGA) were evaluated retrospectively. METHODS OF TESTING: Red-free photographs and sequential digital fluorescein and indocyanine green angiograms obtained by confocal scanning laser ophthalmoscope (the Heidelberg Retina Angiograph; Heidelberg Engineering GmbH, Dossenheim, Germany). MAIN OUTCOME MEASURES: The angiograms were evaluated for the presence of RCA. The following angiographic characteristics were recorded: number and type of anastomoses, location, distance from fovea, area of CNV, presence of pigment epithelium detachment (PED), cystoid macular edema on FA, and intraretinal leakage on ICGA. The direction of flow between the RCA and the CNV was identified by analyzing high-speed angiograms. RESULTS: Retinal choroidal anastomoses were identified in 57 eyes (28%), in 49 of 154 eyes with PED (32%), and in 8 of 51 eyes without PED (16%). Of 109 anastomoses, 70% were venous and 30% were arterial. Ninety-six percent of the eyes had at least one venous anastomosis, 49% of the eyes had an arterial anastomosis, and 46% of the eyes had both. Cystoid macular edema was seen on FA in 37 eyes (65%), and intraretinal indocyanine green leakage was noted in 52 eyes (91%). Twenty-two eyes that underwent high-speed ICGA were analyzed for the direction of flow. All 15 eyes having arterial and venous anastomoses demonstrated a filling pattern from the retinal arteriole to the CNV, followed by the retinal venule. Seven eyes with venous RCA showed flow sequence from the CNV to the collecting retinal venule. CONCLUSIONS: Our study supports the presence of RCA in the early stages of acute exudative AMD with occult CNV, mainly with serous PED. High-speed angiography helps to identify the filling sequence of the RCA and the CNV, and therefore may guide the clinician in planning treatment strategies.

Aged↗
PubMed1997

Indocyanine green angiographic evaluation of retinal pigment epithelial tears.

BACKGROUND: Although choroidal neovascularization has a recognized role in the formation of retinal pigment epithelial tears in the setting of age-related macular degeneration, there frequently was no fluorescein angiographic evidence of choroidal neovascularization in published series. METHODS: Three consecutive patients with a folded retinal pigment epithelium in a subfoveal location, which was associated with a serous macular detachment in the setting of age-related macular degeneration, were studied with intravenous fluorescein angiography and indocyanine green angiography. RESULTS: Fluorescein angiography demonstrated no well-defined choroidal neovascular membrane, although there was evidence of occult choroidal neovascularization. The folded retinal pigment epithelium blocked fluorescence. Indocyanine green angiography demonstrated placoid subfoveal hyperfluorescence consistent with choroidal neovascularization in the region of the folded retinal pigment epithelium and fibrovascular pigment epithelial detachment. Hypofluorescence was noted within the region of the retinal pigment epithelial tear. CONCLUSION: Indocyanine green angiography in our cases clearly demonstrated the presence of presumed choroidal neovascularization in the setting of retinal pigment epithelial tears secondary to age-related macular degeneration.

Aged↗
PubMed1975

Rhegmatogenous retinal detachment after tributary retinal vein occlusion.

Two patients had rhegmatogenous retinal detachment after tributary retinal vein occlusion. Neovascularization adherent to the posterior hyaloid was avulsed, along with a plug of retinal tissue, as the vitreous body collapsed. Localized retinal detachments resulted. Photocoagulation successfully obliterated the retinal holes and prevented extension of the retinal detachments in both cases.

Female↗
PubMed1978

Some observations on ocular manifestation of sickle cell disease.

The ocular manifestations of 76 sickle cell disease patients are reported. Our findings indicate that any type of sickle cell oculopathy may appear in conjunction with any type of hemoglobinopathy and that no single ocular finding is specific to any one type of sickle cell anomaly. Sickle cell oculopathy, particularly retinopathy, is found to be a slowly progressive condition. Treatment of retinal and vitreal neovascularization with photocoagulation seems to be indicated to stop the disease process. Acute retinal vascular occlusion seems to respond favorably to the intravenous administration of low molecular weight dextran and papaverine hydrochloride. Sickle cell patients suffering from retinal detachment do not respond favorably to conventional retinal detachment surgery.

Adult↗
PubMed1998

Increased vascular endothelial growth factor (VEGF) and transforming growth factor beta (TGFbeta) in experimental autoimmune uveoretinitis: upregulation of VEGF without neovascularization.

Experimental autoimmune uveoretinitis (EAU) was induced in Lewis rats and B10.A mice by immunization with S-antigen (S-Ag) to study the potential roles of vascular endothelial growth factor (VEGF) and the beta1 and beta2 isoforms of transforming growth factor (TGFbeta1 and TGFbeta2) during the progression of the disease. VEGF has been implicated as an angiogenic factor in ischemic retinopathies; however, Lewis rats developing EAU have high levels of VEGF in the retina, but no neovascularization. In the present study, immunohistochemical staining for VEGF, TGFbeta1 and TGFbeta2 was performed on the retinas of Lewis rats developing EAU or with oxygen-induced ischemic retinopathy. In rats immunized with S-antigen, a marked upregulation of VEGF was immunohistochemically visualized from the inner nuclear layer to the inner limiting membrane prior to blood-retinal barrier (BRB) failure and lymphocytic infiltration. VEGF is normally induced by hypoxia and its induction leads to neovascularization. Coincident with the increase in VEGF, there was increased immunoreactivity for TGFbeta1 and TGFbeta2 within the same layers of the retina. In contrast, rats with ischemic retinopathy and retinal neovascularization showed only a modest increase in VEGF immunoreactivity, which is largely confined to retinal ganglion cells and inner retinal vessels, and little or no increase in TGFbeta1 or TGFbeta2. In addition, in mice developing EAU, which does not have an abrupt onset as it does in rats and may involve neovascularization, a comparable upregulation of VEGF in the inner retina to that seen in rats developing EAU occurs with no increase in TGFbeta1 or TGFbeta2. Since TGFbeta can inhibit endothelial cell proliferation, it is likely that an increase in TGFbeta may prevent VEGF from exerting its endothelial growth activity in the rat EAU model, but VEGF may be operative in inducing BRB failure. These data suggest that there is a complex interaction among growth factors in the retina and that retinal neovascularization may require an imbalance between stimulatory and inhibitory factors.

Animals↗
PubMed2004

Correlation of optical coherence tomography with angiography in retinal pigment epithelial detachment associated with age-related macular degeneration.

PURPOSE: To correlate optical coherence tomography (OCT) with angiographic signs of choroidal neovascularization (CNV) in retinal pigment epithelial detachment (PED) associated with age-related macular degeneration (ARMD). METHODS: Prospectively, the authors performed OCT in 35 eyes of 35 patients (30 men and 5 women with a mean age of 71.6 years [range, 56-76 years]) with ARMD. All 35 eyes had CNV in the area of PED or adjacent to it, which was shown by fluorescein or indocyanine green angiography. Cross-sectional images were obtained by the OCT scanning line through the CNV and PED. RESULTS: In 10 (56%) of 18 eyes in which the CNV was at the margin of the PED, a small PED was adjacent to the central, dome-shaped PED. There was a notch between the central and small mounds of PED. In 13 (76%) of 17 eyes in which the CNV was within the PED, a notch was seen in the dome-shaped PED, resulting in a contour with 2 mounds. One of the 2 mounds contained a highly reflective mass immediately beneath the detached retinal pigment epithelium in 8 (62%) of the 13 eyes. CONCLUSION: A tomographic notch in the PED may be diagnostically important as an indication of CNV beneath the detached retinal pigment epithelium in eyes with ARMD.

Aged↗