May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Triamcinolone Acetonide Inhibits Retinal Neovascularization Induced by Hypoxic Stimuli
Author Affiliations & Notes
  • N. Kitaya
    Ophthalmology, Asahikawa Medical College, Asahikawa, Japan
  • H. Yokota
    Ophthalmology, Asahikawa Medical College, Asahikawa, Japan
  • R. Sugawara
    Ophthalmology, Asahikawa Medical College, Asahikawa, Japan
  • M. Takeda
    Ophthalmology, Asahikawa Medical College, Asahikawa, Japan
  • A. Takamiya
    Ophthalmology, Asahikawa Medical College, Asahikawa, Japan
  • A. Yoshida
    Ophthalmology, Asahikawa Medical College, Asahikawa, Japan
  • Footnotes
    Commercial Relationships  N. Kitaya, None; H. Yokota, None; R. Sugawara, None; M. Takeda, None; A. Takamiya, None; A. Yoshida, None.
  • Footnotes
    Support  Grant in Aid for Encouragement of Young Scientists from Japan Society for the Promotion of Science
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 549. doi:
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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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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : 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.

Keywords: neovascularization • retina • drug toxicity/drug effects 
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