Clinical and Experimental Studies on Retinal Neovascularization

Patz, Arnall

doi:10.1016/0002-9394(82)90297-5

Cited by 168 publications

(79 citation statements)

References 84 publications

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“…It causes an array of long-term systemic complications [1] . Among these complications is the diabetic retinopathy, which characterized by the increase in capillary permeability [2] , thickening of the basement membrane [3,4] , pericyte necrosis followed by the capillary occlusion, microaneurysms, endothelial cell proliferation, haemorrhage, oedema, neovascularization [5,6] and lately, a fibrous or glial tissue often grows with the vessels to a degree that traction and distortion of the retina may occur, producing retinal damage and retinal detachment [7] and resulting in blindness [8] .…”

Section: Introductionmentioning

confidence: 99%

Sorbitol-Induced Diabetic-Like Retinal Lesions in Rats: Microscopic Study

Ramadan¹

2007

American J. of Pharmacology and Toxicology

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Abstract:The present study investigated the sorbitol toxicity on the retinas of normal albino rats and founded by the light microscope that intra-peritoneal injection of Sorbitol (10-mg/kg-body weight per day) for 24 weeks produced similar diabetic like retinal lesions in these rats. The retinopathic effects of sorbitol injection affect retinal microvessels, pigment epithelium, neural retina and glial cells. Cytoplasmic vacuolation of the pigment epithelium and oedema of the neural retinal cells were evident. Microvascular abnormalities include thick-walled, elongated and dilated blood capillaries. The abnormal capillaries showed aneurysms and were occluded with deformed, fragmented, and adherent blood cells. Another finding was the pyknosis of glial cells. The present investigation concluded that sorbitol is toxic to the retinal tissue and it may play a role in the setup of diabetic retinopathy.

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Section: Introductionmentioning

confidence: 99%

Sorbitol-Induced Diabetic-Like Retinal Lesions in Rats: Microscopic Study

Ramadan¹

2007

American J. of Pharmacology and Toxicology

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“…Neovascularization is considered to be triggered by hypoxic retinal cells that probably produce an angiogenetic factor (Breton et al 1989;Hayreh 1983;Patz 1982), whereas the already dead retinal cells do not have this triggering effect. In the fluorescein angiography it is usually not possible to differ between hypoxic and already dead retinal tissue.…”

Section: Discussionmentioning

confidence: 99%

Fluorescein angiography versus ERG for predicting the prognosis in Central Retinal Vein Occlusion

Larsson

Bauer

Cavallin‐Sjöberg

et al. 1998

Acta Ophthalmologica Scandinavica

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ABSTRACT.Purpose: It is not easy to predict which patients with a central retinal vein occlusion will develop rubeosis and which will not. We have compared two methods for doing so, fluorescein angiography and full-field electroretinogram (ERG). Our aim was to improve our possibilities for predicting rubeosis in patients with central vein occlusion. Methods: 32 patients with a central retinal vein occlusion with a duration of less than 14 days were included in the study. Fluorescein angiography and ERG were performed in all patients. The fluorescein angiograms were studied by two independent examiners in a masked mode. The patients were then followed for at least one year. Results: Development of rubeosis in patients with central retinal vein occlusion could be predicted by fluorescein angiography in 82% of the patients and with ERG in 94% of the patients. The non-ischemic central retinal vein occlusions were identified in 62% by fluorescein angiography and in 100% with ERG. Fluorescein angiography misjudged 9 patients 28%, whereas ERG only misjudged 1 patient, 3%. Conclusion: ERG seems to be a better method for predicting the prognosis in central retinal vein occlusion than fluorescein angiography.

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“…Presumably, the angiogenic growth factors, initially called retinalderived growth factors and later found to be largely aFGF and bFGF (1 5), are contributing to the development of ROP. Observations in infants and experimental animals suggest that retinal ischemia is positively correlated with angiogenesis in OIR (16) and other retinopathies as well (17). The retinopathies develop in unregulated pathologic manners, possibly because of excessive signals for capillary growth.…”

Section: (Mean +mentioning

confidence: 99%

Oxygen-Induced Retinopathy: Lack of Adverse Heparin Effect

Higgins

Phelps

1990

Pediatr Res

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ABSTRACT. Retinopathy of prematurity is a disorder of abnormal retinal vascular proliferation, and one hypothesis for its pathogenesis involves abnormal activity of angiogenic growth factors in the retina. One of these, acidic fibroblast growth factor, is found primarily in retina and brain tissues. Its mitogenic effect is greatly potentiated in vitro by heparin. Because retinopathy of prematurity occurs most often in premature infants who receive the greatest amount of heparin, we tested the hypothesis that heparin may adversely affect the retinopathy observed in kittens after hyperoxic (80% oxygen) exposure. Seventeen litters of kittens were randomly assigned to receive either saline or heparin s.c. injections from d 2 through recovery to 28 d of age; 65 h of high oxygen exposure was started on d 3 to induce a standard retinal injury in our model. There were no differences in the degree of retinopathy between the heparin-treated group [severity score 5.9 f ROP is a vasoproliferative disorder of immature retinal vessels initially described in 1942 (1) and subsequently found to be preserve these lines (13). Therefore, the sickest infants are exposed to more heparin for longer periods of time, and these are the infants at highest risk for ROP. (mean +SDROP results when aberrant retinal vessel regrowth occurs after an initial injury. It has been thought to be driven by ischemic avascular tissue releasing angiogenic growth factors as has recently been demonstrated in the kitten model of OIR (14). Presumably, the angiogenic growth factors, initially called retinalderived growth factors and later found to be largely aFGF and bFGF (1 5), are contributing to the development of ROP. Observations in infants and experimental animals suggest that retinal ischemia is positively correlated with angiogenesis in OIR (16) and other retinopathies as well (17). The retinopathies develop in unregulated pathologic manners, possibly because of excessive signals for capillary growth.Capillary growth and development has been demonstrated to be influenced by several growth factors (18,19). Acidic FGF, found mainly in neural tissue, is relatively abundant in the retina (15), and is mitogenic for a variety of cell types including endothelial cells (20). Significantly, many of the effects of aFGF in vitro are potentiated by heparin or heparin-like molecules (2 1 -23). Acidic FGF activity is potentiated by heparin in vitro (24,25); the importance of size, sulfation, and anticoagulant activity has been described (26). Furthermore, heparin copper-complex has been shown to be angiogenic in vivo (27). Basic FGF is also angiogenic, and has been shown to positively influence capillary growth in vitro but has not been shown to be potentiated by heparin. Other unknown factors may also contribute to abnormal vessel growth in ROP.A logical concern is that widespread heparin use for maintaining central lines and for use in hyperalimentation might exacerbate ROP by potentiating aFGF in vivo. We therefore undertook a study to test the hypothesis that h...

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Clinical and Experimental Studies on Retinal Neovascularization

Cited by 168 publications

References 84 publications

Sorbitol-Induced Diabetic-Like Retinal Lesions in Rats: Microscopic Study

Sorbitol-Induced Diabetic-Like Retinal Lesions in Rats: Microscopic Study

Fluorescein angiography versus ERG for predicting the prognosis in Central Retinal Vein Occlusion

Oxygen-Induced Retinopathy: Lack of Adverse Heparin Effect

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