Abstract
Purpose :
Primary blast injury (PBI) following blast overpressure exposure can affect the eyes and other organs (polytrauma). Yet, relatively little is known about the primary effects to the retina per se. We evaluated the consequences of blast overpressure exposure to the retina using a novel rat model of PBI, under conditions simulating mild traumatic brain injury (mTBI).
Methods :
Group I: Adult male rats exposed to a blast pressure of ~ 63 kPa (~190 dB pSPL), using a custom-built shock tube, with blast wave applied symmetrically (face-on); unexposed age/gender-matched rats were controls (N=3/group). One wk later, one eye per rat was processed for H&E histology and immunohistochemistry, while the contralateral retina was subjected to Western blot (WB) analysis. Tissue sections were probed with primary and fluor-conjugated secondary antibodies, counterstained with DAPI, and imaged by confocal fluorescence microscopy. Group 2: An asymmetrical blast was applied (left side of head); 2 wk post-blast, visual function was assessed by electroretinography (ERG) and optokinetic tracking (OKT: visual acuity (VA) and contrast sensitivity (CS)), and histological analysis of eyes was performed.
Results :
Group 1 (1 wk post-blast): GFAP+ staining was observed in the inner limiting membrane (ILM) and radially throughout the neural retina; only ILM GFAP+ staining was observed in controls. WB analysis of retinas showed ~2-fold increase (p<0.03, t-test) in GFAP in blast-exposed vs. control retinas. Heme oxygenase-1 (HO-1)+ staining was elevated in the RPE, as well as in patches of neural retina, in blast-exposed vs. control rats; however, overt retinal damage was not evident. Group 2 (2 wk post-blast): VA and CS reductions (rel. to controls) were comparable in both eyes, despite blast asymmetry. VA thresholds trended toward reduction (~8-10%) in blast-exposed eyes, reaching statistical significance (p<0.05; 1-way ANOVA) with combined data. ERGs showed no apparent blast-induced rod or cone dysfunction; retinal histology was normal.
Conclusions :
Exposure of rats to mTBI-like PBI conditions results in production of molecular signatures of oxidative stress (HO-1) and reactive gliosis (GFAP) with visual function deficits prior to obvious retinal damage. Involvement of oxidative stress suggests that antioxidants may provide a therapeutic intervention for blast overpressure-induced retinal injury if applied within an appropriate time frame.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.