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N. Kitaya, H. Yokota, R. Sugawara, M. Takeda, A. Takamiya, A. Yoshida; Triamcinolone Acetonide Inhibits Retinal Neovascularization Induced by Hypoxic Stimuli . Invest. Ophthalmol. Vis. Sci. 2003;44(13):549.
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Purpose: Triamcinolone acetonide is a nonsoluble steroid that has recently been used during pars plana vitrectomy to improve visualization of the hyaloid. The inhibitory effects of triamcinolone acetonide on choroidal neovascularization have been reported experimentally and clinically. In the present study, we investigated if triamcinolone acetonide inhibited retinal neovascularization in a retinopathy of prematurity (ROP) model. Methods: Postnatal 7 days (p7) C57BL mice were exposed to 75% oxygen for 5 days. On p12, 10 ul of triamcinolone acetonide (8 mg/ml) was injected into the vitreous cavity with a 30-G needle under a stereomicroscope in 1 eye of each animal returned to room air. The other eyes were injected with the same amount of balanced salt solution (BSS) as the controls. We excluded eyes with vitreous hemorrhage and/or retinal detachment. The animals were sacrificed and the eyes were enucleated on p17. We counted the number of neovascular nuclei extending into the vitreous cavity and prepared whole-mount retinas perfused with high-molecular-weight rhodamine-conjugated dextrans to visualize retinal vessels. Results: The triamcinolone acetonide-treated eyes had a significantly decreased number of neovascular nuclei (n=8) (5.3±2.4) compared with the BSS-treated eyes (n=8) (18.1±13.2) (p<0.05). Whole-mount retinas showed that the vessels in the triamcinolone acetonide-treated eyes were less tortuous and engorged than those in the BSS-treated eyes. Conclusions: This study showed that triamcinolone acetonide inhibits retinal neovascularization and improves the morphologic changes of retinal vessels in an ROP model.
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