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Jae Hyek Choi, Whitney Greene, Mikulas Chavko, Anthony Johnson, Jeffery Cleland, Heuy-Ching Wang; The effects of repeated exposure to low level blast overpressure on rat ocular tissues. Invest. Ophthalmol. Vis. Sci. 2013;54(15):5755. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
Blast-induced ocular injury is a frequent cause of morbidity for survivors of improvised explosive devices (IEDs). A single exposure to a moderate level of blast overpressure (BOP) has been shown to cause damage to the eye in a rat model; however, during combat, military personnel may in fact be exposed to low levels of BOP multiple times. The purpose of this study is to characterize the effects of repeated exposure to low level BOP on rat ocular tissues. The pathophysiology of blast-induced ocular injury was examined by analysis of activated caspase 3 and expression of glial fibrillary acidic protein (GFAP) in ocular tissues from rats exposed five times to low level BOP.
A compressed air shock tube was used to deliver 70±7 KPa BOP of duration 2 ms to the frontal side of rats. Rats were exposed once daily for five days then euthanized on day 5, one hour after the last blast exposure. Rats subjected to a single blast exposure euthanized at 5 days after blast exposure and rats not exposed to blast were included as controls. Ocular tissues were collected and processed for immunohistochemistry to detect activated caspase 3 and GFAP. The number of positive cells was quantified
Activated caspase 3 was detected in the retina and optic nerve from all animals subjected to BOP exposure, whether one time exposure or repeated exposures. Similar levels of activated caspase 3 were detected in the ganglion layer (GL) and inner nuclear layer (INL) of the retina. Animals that had received repeated BOP exposures had significantly higher levels of activated caspase 3 in the optic nerve. In all animals subjected to BOP exposure, GFAP immunoreactivity was detected in the retinal Muller cells traversing the INL to the outer plexiform layer (OPL), while the central regions of the retina were negative for GFAP. Tissues from control animals not exposed to BOP were negative for activated caspase 3 and GFAP.
Both single exposure and repeat exposure to low level BOP resulted in damage to the retina in the GL and the INL. Repeated exposure to BOP caused increased apoptosis in the optic nerve as indicated by activated caspase 3, suggesting that repeated exposure to BOP causes more severe optic neuropathy than a single BOP exposure. Exposure to BOP caused a distinct pattern of gliosis at the periphery of the retina as indicated by GFAP immunoreactivity.
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