November 1997
Volume 38, Issue 12
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Articles  |   November 1997
Retinal toxicity of nitric oxide released by administration of a nitric oxide donor in the albino rabbit.
Author Affiliations
  • H Oku
    Department of Ophthalmology, Osaka Medical College, Takatsuki, Japan.
  • H Yamaguchi
    Department of Ophthalmology, Osaka Medical College, Takatsuki, Japan.
  • T Sugiyama
    Department of Ophthalmology, Osaka Medical College, Takatsuki, Japan.
  • S Kojima
    Department of Ophthalmology, Osaka Medical College, Takatsuki, Japan.
  • M Ota
    Department of Ophthalmology, Osaka Medical College, Takatsuki, Japan.
  • I Azuma
    Department of Ophthalmology, Osaka Medical College, Takatsuki, Japan.
Investigative Ophthalmology & Visual Science November 1997, Vol.38, 2540-2544. doi:
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    • Get Citation

      H Oku, H Yamaguchi, T Sugiyama, S Kojima, M Ota, I Azuma; Retinal toxicity of nitric oxide released by administration of a nitric oxide donor in the albino rabbit.. Invest. Ophthalmol. Vis. Sci. 1997;38(12):2540-2544.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

PURPOSE: Nitric oxide (NO), which has been identified as an endothelium-derived relaxing factor, might be involved in regulation of retinal circulation and intraocular pressure. Recently, it was suggested that NO might also be related to neuronal excitotoxicity mediated by the N-methyl-D-aspartate receptor and to the pathologic changes induced by some kinds of uveitis. However, ocular toxicity of NO released by an NO donor has not been clearly demonstrated. In the current study, NO neurotoxicity in the retina was investigated. METHODS: S-nitroso-N-acetyl-DL-penicillamine (SNAP, 200 nmol) was injected into the vitreous of albino rabbits as an NO donor. The changes of retinal function were evaluated at 1, 2, and 3 hours and 1 and 4 weeks after SNAP injection, using electroretinogram and visual-evoked potentials. Histologic changes of the retina were also examined. RESULTS: Injection of SNAP reduced the a-wave amplitude. In contrast, the amplitudes of the oscillatory potentials were increased during the 3-hour observation period. Histologic examination showed vacuolar degeneration and loss of the nuclei of the photoreceptors. In the inner retina, some ganglion cells were lost, and cell density in the internal nuclear layer was decreased. CONCLUSION: Retinal toxicity of NO was demonstrated functionally and histologically, suggesting that NO may play a pathophysiologic role in retinal ischemia or in degenerative retinal diseases.

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