May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Protective Effect of Hydrogen in Retinal Ischemia-Reperfusion Injury
Author Affiliations & Notes
  • H. Oharazawa
    Dept of Ophthamology, Nippon Medical School Musashikosugi Hospital, Kawasaki, Japan
  • I. Osawa
    Department of Biochemistry and Cell Biology, Institute of Development and Aging Sciences, Graduate School of Medicine, Nippon Medical School, Kawasaki, Japan
  • T. Igarashi
    Dept of Ophthamology, Nippon Medical School, Tokyo, Japan
  • M. Ishikawa
    Department of Biochemistry and Cell Biology, Institute of Development and Aging Sciences, Graduate School of Medicine, Nippon Medical School, Kawasaki, Japan
  • H. Fujii
    Dept of Ophthamology, Nippon Medical School Musashikosugi Hospital, Kawasaki, Japan
  • H. Suzuki
    Dept of Ophthamology, Nippon Medical School, Tokyo, Japan
  • H. Takahashi
    Dept of Ophthamology, Nippon Medical School, Tokyo, Japan
  • S. Ohta
    Department of Biochemistry and Cell Biology, Institute of Development and Aging Sciences, Graduate School of Medicine, Nippon Medical School, Kawasaki, Japan
  • Footnotes
    Commercial Relationships  H. Oharazawa, None; I. Osawa, None; T. Igarashi, None; M. Ishikawa, None; H. Fujii, None; H. Suzuki, None; H. Takahashi, None; S. Ohta, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 6121. doi:
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      H. Oharazawa, I. Osawa, T. Igarashi, M. Ishikawa, H. Fujii, H. Suzuki, H. Takahashi, S. Ohta; Protective Effect of Hydrogen in Retinal Ischemia-Reperfusion Injury. Invest. Ophthalmol. Vis. Sci. 2008;49(13):6121.

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

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Abstract

Purpose: : The retinal ischemia-reperfusion model is known to induce apoptosis of cells and significant reductions in thickness in all layers of the retina. These features closely resemble those after retinal ischemic insult and acute glaucoma. Some studies have demonstrated that oxygen-derived free radicals generated during ischemia and on reperfusion may trigger ischemic cell damage in the retina. Recently, it was shown that hydrogen (H2) markedly decreased oxidative stress and suppressed brain injury caused by ischemia and reperfusion. In this study, we investigated the protective effects of H2 in retinal ischemia-reperfusion model in rat.

Methods: : Retinal ischemia was induced in Sprague-Dawley rats (200~250 g) by elevating the intraocular pressure (IOP) through the insertion of a needle into the anterior chamber connected to a saline reservoir. IOP was raised to 110 mmHg for 60 min. To investigate the neuroprotective effects of H2, the rats were applied continuous eyedrops of H2 saturated normal saline solution or normal saline control from the onset of ischemia to 30 min after reperfusion. The eyes were enucleated 1 week after reperfusion and fixed in 1% glutaraldehyde and 4% paraformaldehyde in 0.1 M phosphate buffered saline. Sections were cut along the vertical meridian of the eye and passed through the optic nerve head and stained with hematoxylin and eosin. The retinal damage was assessed by measuring the inner retinal thickness (IRT).

Results: : The mean thickness of IRT in control rats and that of H2 treated rats was 63.6 ± 7.2 µm and 100 ± 1.4 µm, respectively (P < 0.01). The eyedrops of H2 saturated normal saline solution significantly inhibited the reduction of IRT.

Conclusions: : Our result suggests that the eyedrops of H2 saturated normal saline solution plays an important role to protect neurons in retinal ischemia-reperfusion injury and may be useful for such as acute glaucoma, acute retinal vascular occlusion and diabetic retinopathy.

Keywords: retina • ischemia • oxidation/oxidative or free radical damage 
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