
To examine the effect lf light on retinal neovascularization and vasculogenesis in a reproducible and quantifiable model of oxygen-induced proliferative retinopathy in the mouse.C57Bl/6J mice were reared in room air, 68% oxygen, or 75% oxygen and were exposed to darkness, low cyclical light (200-350 lux), or high-intensity continuous light (3000-4500 lux). The entire retinal vascular pattern was visualized in fluorescein-dextran perfused flat-mount preparations. Proliferative retinopathy was quantified by counting neovascular nuclei in 6 microns cross-sections of whole eyes.Light exposure did not exacerbate the proliferative retinopathy that was seen after 68% oxygen exposure, which induced a meager proliferative response, nor after 75% oxygen exposure, which induced an exuberant proliferative response. In room air, retinas from all three illumination groups had normal vascular patterns.In this model of oxygen-induced retinopathy, under the conditions tested, light neither exacerbated the hyperoxia-induced neovascularization nor affected normal retinal vascular development.
Light, Fundus Oculi, Infant, Newborn, Retinal Vessels, Dark Adaptation, Dextrans, Fluoresceins, Mice, Inbred C57BL, Perfusion, Disease Models, Animal, Mice, Random Allocation, Animals, Humans, Retinopathy of Prematurity, Fluorescein Angiography
Light, Fundus Oculi, Infant, Newborn, Retinal Vessels, Dark Adaptation, Dextrans, Fluoresceins, Mice, Inbred C57BL, Perfusion, Disease Models, Animal, Mice, Random Allocation, Animals, Humans, Retinopathy of Prematurity, Fluorescein Angiography
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