April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Bevacizumab Treatment in a Rodent Model of Non-Arteritic Ischemic Optic Neuropathy (rAION)
Author Affiliations & Notes
  • G. S. Reilly
    Department of Ophthalmology, University of Maryland, Baltimore, Maryland
  • S. L. Bernstein
    Ophthalmology, Anatomy and Neurobiology, Genetics, University of Maryland School of Medicine, Baltimore, Maryland
  • Y. Guo
    Department of Ophthalmology, University of Maryland, Baltimore, Maryland
  • Footnotes
    Commercial Relationships  G.S. Reilly, Genentech Inc provided reagents (rodent anti VEGF and control), F; S.L. Bernstein, Genentech Inc provided reagents (rodent anti VEGF and control), F; Y. Guo, Genentech Inc provided reagents (rodent anti VEGF and control), F.
  • Footnotes
    Support  SLB: Supported by NIH grants RO1-EY019529 and 2RO1-EY015304
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 1456. doi:
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    • Get Citation

      G. S. Reilly, S. L. Bernstein, Y. Guo; Bevacizumab Treatment in a Rodent Model of Non-Arteritic Ischemic Optic Neuropathy (rAION). Invest. Ophthalmol. Vis. Sci. 2010;51(13):1456.

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

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Abstract

Purpose: : Bevacizumab (Lucentis) has been proposed as a clinical treatment for non-arteritic ischemic optic neuropathy (NAION). Rodent anterior ischemic optic neuropathy (rAION) is a model that has been established to having many similarities to human NAION. This study utilized this model in order to test whether Bevacizumab is potentially effective in improving outcomes in NAION.

Methods: : All animal protocols were approved by the Institutional Animal Use and Care Committee (IACUC). A murinized form of Bevacizumab (rodent Lucentis) and antibody control were obtained from Genentech Inc (San Francisco, CA). The retinal fundi of six male Sprague-Dawley rats (120-150g) were photographed. rAION was induced in both eyes of three animals (Treatment Group) and one eye of an additional three animals (Naïve Controls). Immediately after induction of the bilaterally treated animals, one eye of each animal intravitreally received 10ug of an Avastin-VEGF homologue B20-4.1.1 VEGF:5563. The other eye received 10ug of a control (ragweed) antibody. The naïve controls were left uninjected. Eyes were photographed 2 days post-induction, immediately prior to euthanasia and enucleation. Eyes were fixed in 4% paraformaldehyde-phosphate-buffered saline (PF-PBS) for histologic analysis. Longitudinal optic nerve sections including the intraretinal portion of the optic nerve (ON) were obtained for analysis. ON sections were examined and compared for edema and evidence of peripapillary retinal displacement

Results: : There was no significant decrease in gross optic nerve edema in rodent Bevacizumab-treated rAION induced eyes at 2 days post-treatment. No significant differences were found on microscopic examination.

Conclusions: : Bevacizumab in this limited study does not seem to directly improve optic nerve edema associated with rAION. However, because of the limited number of animals and relatively gross method of initial determination of ON edema, future studies with more animals will assess Bevacizumab and optic nerve edema in rAION utilizing the Heidelberg Retina Angiograph (HRA).

Keywords: vascular endothelial growth factor • optic nerve • ischemia 
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