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Chunyi Shao, Weijie Zhang, Yang Hu, Linna Lu, Yan Liu, Yao Fu, Xianqun Fan; A rabbit model of corneal endothelial injury using the Nd:YAG laser. Invest. Ophthalmol. Vis. Sci. 2016;57(12):5302.
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© ARVO (1962-2015); The Authors (2016-present)
Several animal models of corneal endothelial decompensation have been reported in the literature including cryoinjury-induced, chemical-induced, and mechanical scraping-induced corneal endothelial decompensation. However, all existing models have drawbacks such as damage to intraocular structures, invasiveness, and difficulty. In this study, we proposed a new rabbit model of corneal endothelial injury using neodymium-doped yttrium aluminum garnet (Nd:YAG) laser.
Corneal endothelium of 6 rabbits was treated with a Nd:YAG laser in a scattered fashion using the Abraham capsulotomy lens and a pulse energy of 3-5 mJ. The energy was delivered as a single pulse per burst. Corneas were examined for edema using a slit lamp biomicroscope and images were taken before, right after, and 1, 2 and 3 weeks after treatment. Confocal microscopy, optical coherence tomography (OCT), and rebound tonometer were also applied to assess endothelial cells, cornea thickness, intraocular pressure (IOP), respectively.
The corneal endothelial defect was observed using confocal microscopy, which manifested as dotted or focal defects. The stroma was intact. The cornea had minimal edema immediately after laser application, which increased to complete opacity at 1 week after laser treatment. Corneal thickness was dramatically increased at 1 week after laser treatment. All corneas failed to regain transparency 3 weeks after laser. We observed no damage to intraocular structures.
Nd:YAG laser can effectively induce bullous keratopathy in rabbits. The procedure is simple, reproducible, and retains the normal intraocular structures. More importantly, this model induces corneal endothelial dysfunction, but avoids total destruction of endothelial cells. This study provides a promising model to further study endothelial cell damage and to develop new therapies.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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