December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Neuroprotective Action of Nipradilol in a Rat Model of Optic Nerve Degeneration
Author Affiliations & Notes
  • A Sawada
    Ophthalmology Gifu Univ School of Medicine Gifu Japan
  • MZ Karim
    Ophthalmology Gifu Univ School of Medicine Gifu Japan
  • K Mizuno
    Pharmacology Tokyo Research Laboratories Kowa Company Ltd Tokyo Japan
  • H Kawakami
    Ophthalmology Gifu Univ School of Medicine Gifu Japan
  • T Yamamoto
    Ophthalmology Gifu Univ School of Medicine Gifu Japan
  • Footnotes
    Commercial Relationships   A. Sawada, None; M.Z. Karim, None; K. Mizuno, Kowa Company, Ltd E; H. Kawakami, None; T. Yamamoto, None. Grant Identification: Supported by a Grant-in-Aid for scientific research from Ministry of Education, Culture, Sports, Sci
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 2203. doi:
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      A Sawada, MZ Karim, K Mizuno, H Kawakami, T Yamamoto; Neuroprotective Action of Nipradilol in a Rat Model of Optic Nerve Degeneration . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2203.

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

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Abstract

Abstract: : Purpose: Recently nipradilol, an α1, ß-blocker with a nitric oxide donative action, is used as an ocular hypotensive agent for glaucoma patients in Japan. The aim of the present study was to investigate the neuroprotective effect of nipradilol on the optic nerve injury in the rat. Methods: . Using a calibrated forceps, a crush lesion inflicted unilaterally on the optic nerve 2 mm behind the globe of adult Wistar albino rats was followed by a topical instillation of either (0.25%) nipradilol or vehicle against both eyes twice daily until sacrifice. A sham operation was conducted to the contralateral eyes. Intraocular pressure (IOP) measurement was performed before and 4,7,14,21,28 days after acute injury. One week before sacrifice, Fluoro-Gold (FG) was injected into superior colliculi bilaterally to identify surviving retinal ganglion cells (RGCs). Approximately one month after injury, retinal damage was assessed by counting FG-labeled RGCs. Results: In both groups, IOP in crush eyes slightly, however, statistical significantly elevated compared with sham-operated contralateral eyes during all follow-up periods. There was no significant difference in IOP of both eyes between the nipradilol and control groups. Within one month, in the control group the mean RGC density decreased to 75% of the contralateral eyes. While, the optic nerve crush with topical application of nipradilol showed a considerably smaller decrease in mean RGCs to 89%. Conclusion: Our findings might indicate that nipradilol can alleviate RGC death induced by optic crush injury in the rat.

Keywords: 316 animal model • 415 ganglion cells • 489 neuroprotection 
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