June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Treatment with non-medicated eye drops reduces damage caused by blast exposure
Author Affiliations & Notes
  • Courtney Bricker-Anthony
    Vanderbilt Eye Institute, Vanderbilt University, Nashville, TN
    Vanderbilt Brain Institute, Vanderbilt University, Nashville, TN
  • Tonia S Rex
    Vanderbilt Eye Institute, Vanderbilt University, Nashville, TN
    Vanderbilt Brain Institute, Vanderbilt University, Nashville, TN
  • Footnotes
    Commercial Relationships Courtney Bricker-Anthony, None; Tonia Rex, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 6027. doi:
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      Courtney Bricker-Anthony, Tonia S Rex; Treatment with non-medicated eye drops reduces damage caused by blast exposure. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):6027.

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

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Abstract

Purpose: To determine if treatment with non-medicated eye drops immediately after blast exposure reduces both corneal and retinal pathology.

Methods: We exposed the left eyes of 3 month-old DBA/2J mice to a single, 26psi blast of compressed air and provided a subset of mice with non-medicated eye drops (treated). Mice were collected at 3 and 28 days post-injury. All eyes were cryo-embedded, sectioned and labeled with antibodies against GFAP, Iba1, nitrotyrosine and TUNEL. Additional sections were stained with hematoxylin and eosin to examine structure. Optic nerves were embedded in resin, sectioned and stained with p-phenylenediamine.

Results: The majority (90%) of untreated (blast exposed, no eye drops) corneas contained numerous pathologies (edema, hyphema, neovascularization), while only about 10% of corneas from treated eyes were edematous. Immune infiltrate were present in both the anterior and posterior chamber of untreated eyes but was limited to the subretinal space in treated eyes. RPE vacuolization was also less frequent and less severe in treated eyes. Nitrotyrosine immunolabeling and reactive microglia were limited to focal regions in the mid-peripheral and central retina of treated eyes as compared to widespread reactivity in untreated eyes. There was no difference in TUNEL, GFAP immunolabeling, or optic nerve pathology between treated and untreated eyes.

Conclusions: An over-pressure air-wave induces corneal damage that can lead to ocular inflammation. This damage and inflammation was mostly prevented by acute treatment with viscous eye drops, which served to temporarily restore the tear film and prevent exposure keratopathy. This study shows that much of the RPE pathology and retinal oxidative stress was a result of the ocular inflammation. However, the photoreceptor cell death and optic nerve damage was unaffected by the eye drops suggesting that this pathology was due to the blast wave itself.

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