April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
An Experimental Model of Optic Nerve Head Injury
Author Affiliations & Notes
  • Dimosthenis Mantopoulos
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, MA
    Ophthalmology, Ohio State University, Columbus, OH
  • Athanassios Tsakris
    Microbiology, Athens Medical School, Athens, Greece
  • Basil S Pawlyk
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, MA
  • Michael A Sandberg
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, MA
  • Joan W Miller
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, MA
  • Joseph F Rizzo
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, MA
  • Demetrios G Vavvas
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, MA
  • Dean M Cestari
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, MA
  • Footnotes
    Commercial Relationships Dimosthenis Mantopoulos, None; Athanassios Tsakris, None; Basil Pawlyk, None; Michael Sandberg, None; Joan Miller, None; Joseph Rizzo, None; Demetrios Vavvas, None; Dean Cestari, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 6222. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Dimosthenis Mantopoulos, Athanassios Tsakris, Basil S Pawlyk, Michael A Sandberg, Joan W Miller, Joseph F Rizzo, Demetrios G Vavvas, Dean M Cestari; An Experimental Model of Optic Nerve Head Injury. Invest. Ophthalmol. Vis. Sci. 2014;55(13):6222.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: Optic nerve head ischemia is the result of decreased vascular perfusion secondary to a number of mechanisms, inflammatory or not, the common outcome of which can be vision loss for the patient. In order to study the disease mechanism as well as neuroprotective modalities, experimental tools are valuable. Here, we present a new experimental model of optic nerve head injury.

Methods: Photodynamic treatment was applied to the optic disc of Brown-Norway rats after intraperitoneal injection of mesoporphyrin IX. Imaging with fluorescein angiography (FA) and spectral domain optical coherence tomography (SD-OCT) was followed by immunohistorchemistry (TUNEL and CD68+) and ELISA analysis. Electrophysiology (Visual Evoked Potentials) was used to evaluate functional changes.

Results: FA findings were significant for early disc hyperfluorescence and late leakage, while SD-OCT detected optic nerve edema and accumulation of subretinal fluid. Apoptotic cell death in the ganglion cell layer was statistically significant from day 1 (12.5 ± 6.7, p < 0.01) and peaked on day 7 (60.75 ± 15.21, p < 0.01). Monocytes/macrophages positive for CD68+ were also found elevated with a peak on day 7 (r = 10.2- fold, p < 0.05). Macrophage Chemoattractant Protein 1 (MCP- 1) and Macrophage Inflammatory Protein 2 (MIP- 2) were upregulated at different timepoints. Finally, VEPs were significant for reductions in amplitude and delay in implicit time.

Conclusions: Mesoporphyrin IX can be used for a photodynamically induced model of optic nerve head injury with resultant histologic and electrophysiologic changes. Given the long half-life of Mesoporphyrin IX and the ease of intraperitoneal injections this experimental model may offer advantages for future neuroprotective studies.

Keywords: 613 neuro-ophthalmology: optic nerve • 647 photodynamic therapy • 615 neuroprotection  
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×