Abstract
Purpose:
To characterize the ultrastructural morphology of retinal neovascularization secondary to light-induced retinal damage in albino rats.
Methods:
Eyes from 5 adult female Albino Wistar rats exposed to 12h of cyclic diffuse cool white 3,000 lux intensity light for 1 month were enucleated after two months of exposure to ambient light and fixed in 2.5% glutaraldehyde. The posterior segments of the globes were routinely processed for transmission electron microscopy.
Results:
All animals presented lesions consistent with chronic light-induced retinopathy, e.g., complete loss of photoreceptors and atrophy of the outer plexiform layer with the inner nuclear layer directly contacting RPE. Multiple vascular profiles traversed the inner plexiform and nuclear layers, contacting hyperplastic RPE that proliferated along the length of the vessels. In other areas RPE was attenuated and vessels came in close proximity to Bruch’s membrane. Proliferating vessels were small (5-15μm in diameter), with patent lumen and formed clusters that were denser near RPE. Vessels presented 3 distinct phenotypes. The first type, consistent with a retinal phenotype, presented complete luminal coverage with robust endothelial cells, tight junctions, thick (100-300 nm) basement membrane and pericytes. The second type, resembling choriocapillaris, presented delicate endothelium with fenestrations, thin (20-50 nm), irregular and discontinuous basement membrane and no pericyte coverage. The third type presented mix features of retinal and choriocapillaris phenotype with thick basement membranes, endothelial cell tight junctions and fenestrations and variable pericyte coverage. Even after multiple step sections through the tissues we did not visualize vascular profiles crossing Bruch’s membrane and/or extending into the choriocapillaris in any of the samples analyzed.
Conclusions:
Chronic retinal light induced retinopathy in rats is characterized by severe atrophy of the outer retina and neovascular proliferation. As the retina atrophies the proliferating vessels get in close contact with RPE. We hypothesize that the variations in vascular morphology reported are driven by the changes in the perivascular environment and close proximity to RPE cells. Understanding this phenomenon of vascular morphology shift can be beneficial not only to basic vascular research but also to clinical ocular neovascular diseases.
Keywords: 597 microscopy: electron microscopy •
700 retinal neovascularization •
695 retinal degenerations: cell biology