September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Acute ocular edema in survivable primary blast induced ocular injury in rabbits
Author Affiliations & Notes
  • J. David Rios
    Ocular Trauma Research Task Area, U.S. Army Institute of Surgical Research, San Antonio, Texas, United States
  • Jae-Hyek Choi
    Multi Organ Support Task Area,, U.S. Army Institute of Surgical Research, JBSA Fort Sam Houston, San Antonio, Texas, United States
  • Jennifer McDaniel
    Ocular Trauma Research Task Area, U.S. Army Institute of Surgical Research, San Antonio, Texas, United States
  • Brian Lund
    Ocular Trauma Research Task Area, U.S. Army Institute of Surgical Research, San Antonio, Texas, United States
  • Footnotes
    Commercial Relationships   J. David Rios, None; Jae-Hyek Choi, None; Jennifer McDaniel, None; Brian Lund, None
  • Footnotes
    Support  Department of Defense Vision Research Program, Award Number W81XWH-12-2-0055
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 740. doi:
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    • Get Citation

      J. David Rios, Jae-Hyek Choi, Jennifer McDaniel, Brian Lund; Acute ocular edema in survivable primary blast induced ocular injury in rabbits. Invest. Ophthalmol. Vis. Sci. 2016;57(12):740.

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

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Abstract

Purpose : Recently we reported corneal and retinal thickness induced by low level blast exposure. However, the underlying mechanism of this blast-induced effect on the corneal and retinal tissues remains unclear. We hypothesize that the expression of markers that are linked to corneal and retinal injuries such as the edema-regulating proteins; aquaporin-4 and -5 (AQP4 and AQP5) and the intermediate filament protein (GFAP) would be altered following primary blast-induced injury.

Methods : Adult male Dutch Belted rabbits were anesthetized and then exposed to blast waves with peak overpressures of 51.2-53.0 kPa (~8 psi), 78.8-88.7 kPa (~12 psi), and 120.4-132.1 kPa (~17 psi). These three exposure groups experienced peak blast overpressure specific impulses (impulse per unit surface area) of 56.0-59.3 kPa-ms (8.12-8.60 psi-ms), 96.5-104.3 kPa-ms (14.0-15.1 psi-ms) and 141.6-158.5 kPa-ms (20.5-23.0 psi-ms). Unexposed rabbits were included as controls. Animals were then euthanized at 48 h post exposure. Immunohistochemistry using a combination of AQP4, AQP5 and GFAP antibodies was employed to follow changes in the cornea, retina and optic nerve.

Results : The cornea and retina showed increase in AQP4 with corresponding peak blast wave overpressures of 119 kPa as compared to controls. AQP5 expression also increased in corneal epithelium after 119 kPa blast exposure. Increased expression of GFAP was also detected only in the optic chiasm in 119 kPa blast exposed rabbits. No changes in the expression of AQP4, AQP5, and GFAP were observed from either unexposed controls or lower-level blast exposed rabbits.

Conclusions : Survivable primary blast exposure resulted in edema-related changes in the cornea and retina, manifested by the increased expression of AQP4 and AQP5 with blast overpressure specific impulses. Changes in the expression of these markers confirm recent observations where corneal and retinal thicknesses were induced by low level blast exposure in a rabbit model. Increased GFAP expression in optic nerve chiasm also suggests optic nerves gliosis. These findings support potential acute injury mechanisms in which increased water permeability and microglial activation are caused by primary blast exposure. Further studies to confirm this observation are warranted to elucidate the underlying mechanisms and potential role of these biomarkers on the effect of acute primary blast exposure in the corneal and retinal tissues.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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