May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Amelioration of Endothelin–1 Induced Optic Nerve Head Ischemia by Topical Bunazosin.
Author Affiliations & Notes
  • H. Oku
    Ophthalmology, Osaka Medical College, Takatsuki, Japan
  • W. Goto
    Ophthalmology, Osaka Medical College, Takatsuki, Japan
  • T. Okuno
    Ophthalmology, Osaka Medical College, Takatsuki, Japan
  • T. Sugiyama
    Ophthalmology, Osaka Medical College, Takatsuki, Japan
  • T. Ikeda
    Ophthalmology, Osaka Medical College, Takatsuki, Japan
  • Footnotes
    Commercial Relationships  H. Oku, None; W. Goto, None; T. Okuno, None; T. Sugiyama, None; T. Ikeda, None.
  • Footnotes
    Support  none
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 2154. doi:
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      H. Oku, W. Goto, T. Okuno, T. Sugiyama, T. Ikeda; Amelioration of Endothelin–1 Induced Optic Nerve Head Ischemia by Topical Bunazosin. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):2154.

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

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Abstract

Abstract: : Purpose: To investigate the effects of bunazosin hydrochloride, α1–adrenergic blocker, on the impairment of optic nerve head (ONH) blood flow and depression of visual function caused by repeated intravitreal injection of endothelin–1 (ET–1) in rabbits. Methods: We injected ET–1 (20 pmol) into the right posterior vitreous of rabbits twice a week for 4 weeks, and the subsequent observation period was set at 8 weeks. The animals which received ET–1 were divided into two groups; one group was given topical 0.01% bunazosin (ET–1 + bunazosin–treated group), and the second group was given vehicle for bunazosin (ET–1 + bunazosin vehicle–treated group) twice a day for 8 weeks. The ONH blood flow was monitored using laser speckle method, and the visual function was determined by visually–evoked potentials (VEPs). Changes in the ONH cup/disk area, and in the number of cells in the retinal ganglion cell layer (GCL) were also determined. Results: Repeated injections of ET–1 decreased the ONH blood flow by 30% or more, prolonged the VEP implicit time, enlarged the optic cup and decreased the number of GCL cells in the ET–1 + bunazosin vehicle–treated group. Topical bunazosin significantly decreased these impairments induced by ET–1. Conclusions: These results indicate that topical bunazosin suppresses the changes in ONH circulation and function induced by intravitreal ET–1.

Keywords: pharmacology • ischemia • electrophysiology: non–clinical 
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