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J. I. Patel, P. K. Yu, I. L. McAllister, S. Cringle, D.-Y. Yu; Choroidal Neovascularization in the Rodent Model: Induction by 810nm Laser. Invest. Ophthalmol. Vis. Sci. 2007;48(13):1473. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
To date laser-induction of choroidal neovascularization (CNV) has used wavelengths from 488 to 647nm in a rodent model. We investigated whether CNV formation can be induced with an 810nm laser in this same model.
Both eyes of six Adult male Brown-Norway rats (BN) were lasered with an 810nm wavelength at varying powers (from 200 to 720mw) (constant time (100ms) and spot size (0.3mm). We examined the time course of histological development of CNV by sacrificing the animals at days 1, 3, 7 and 15 with the eyes fixed and snap frozen for cryosectioning and stained with haemotoxylin & eosin, VEGF immunochemistry and endothelial cells.
Laser powers from 200 to 400 mw (lower powers) produced a grey-white retinal reaction whilst powers from 550 to 720 mw (higher powers) caused immediate choroidal bleeding. At day 1 and day 3, the higher powers produce a lesion disrupting the outer retina with a few vascular lumen, discontinuity of the retinal pigment epithelium (RPE) and VEGF staining at the inner limiting membrane (ILM) (reactive VEGF staining) but none within the lesion. At day 7, the lower powers produce a lesion which demonstrates a continuous RPE layer, both reactive VEGF staining and mild staining within the lesion with vascular lumen whilst the higher powers produce a similar lesion as before but with greater fibrosis. At day 15, with the lower powers (especially 250 and 300mw) the lesion shows discontinuity of the RPE layer, vascular lumen and moderate degree of VEGF staining within the lesion with disruption of the outer retina. The higher powers produce a similar effect as seen at previous time points. With all powers, choroidal neovascularization with vascular lumen were seen beginning at day 3.
In this rodent model, 810nm laser can induce choroidal neovascularization after day 3 with vascular lumen, VEGF staining within the lesion from day 15 and at lower powers (250 and 300mw) the RPE layer was intact then later (at 14 days) becomes discontinuous as the CNV develops. At these lower powers with an initial intact RPE layer, the choroidal neovascularization maybe induced by intact RPE rather than from ruptured Bruch’s membrane which maybe implied from immediate choroidal bleeding seen with the higher powers used. Present laser-induced models rely on the rupture of Bruch’s membrane to induce CNV.
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