May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Neuroprotection by Brimonidine Treatment in a Rat Model of Anterior Ischemic Optic Neuropathy
Author Affiliations & Notes
  • N. Danylkova
    Ophthalmology, University of Minnesota, Minneapolis, MN
  • H.D. Pomeranz
    Ophthalmology, University of Minnesota, Minneapolis, MN
  • S.R. Alcala
    Ophthalmology, University of Minnesota, Minneapolis, MN
  • Y. Sadeghi
    Ophthalmology, University of Minnesota, Minneapolis, MN
  • L.K. McLoon
    Ophthalmology, University of Minnesota, Minneapolis, MN
  • Footnotes
    Commercial Relationships  N. Danylkova, None; H.D. Pomeranz, None; S.R. Alcala, None; Y. Sadeghi, None; L.K. McLoon, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 668. doi:
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      N. Danylkova, H.D. Pomeranz, S.R. Alcala, Y. Sadeghi, L.K. McLoon; Neuroprotection by Brimonidine Treatment in a Rat Model of Anterior Ischemic Optic Neuropathy . Invest. Ophthalmol. Vis. Sci. 2005;46(13):668.

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

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Abstract

Abstract: : Purpose: Alpha–2 agonists have demonstrated neuroprotective ability in various glaucoma and ischemia–reperfusion injury models. The purpose of this study was to evaluate the possible long–term neuroprotective effect of brimonidine (an alpha–2 agonist) in a rodent model of anterior ischemic optic neuropathy (AION). Methods: Adult female Long Evans rats were divided into 4 experimental groups. An experimental anterior ischemic optic neuropathy was induced by an injection of Rose–Bengal dye into the tail vein, followed by argon green laser beam treatment of the vessels at the optic disc area of the right eye with intensity of 12 pulses, at 100 microWatts each. The left eye served as a control. Group 1 received topical treatment with 0.15% brimonidine tartrate twice a day for 7 days before the injury; Group 2 received topical treatment with brimonidine twice daily for 14 days following the induction of optic nerve ischemia; Groups 3 and 4 received topical 0.9% NaCl treatment either 7 days before or 14 days after injury. Animals were sacrificed 4 months after the injury. Harvested tissue was embedded in resin, sectioned at 1 micron, and stained for quantitative analysis. Two random cross–sections of each optic nerve were chosen for axon counting. Results: Laser–induced optic nerve ischemia resulted in a 70 (+/– 5%) loss of optic axons compared to controls. In those rats pretreated with topical brimonidine prior to optic nerve ischemia, there was a 60% increase in long–term axonal survival compared to the controls. In the rats treated with topical brimonidine after the optic nerve ischemia, the increase in axonal survival in the injured optic nerves was 35 (+/– 7 %) greater than that seen after laser–induced injury alone. Conclusions: Our findings suggest that brimonidine treatment may promote axonal survival in the optic nerve of rat eyes subjected to ischemia–reperfusion injury. Furthermore, treatment with the brimonidine prior to the ischemic injury results in a greater axonal survival rate than treatment given after the induction of optic nerve ischemia. These results suggest that brimonidine may have potential use for prevention of AION as well as for its treatment.

Keywords: neuro-ophthalmology: optic nerve • neuroprotection • ischemia 
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