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J. David Rios, Sandra Becera, Josianne Babineaux, Peter Johnson, Peter Edsall, William Elliott, Nathan Wienandt, Ammon W Brown, Brian Lund; Primary blast overpressure causes pathological changes on retina and optic nerve in a rat model. Invest. Ophthalmol. Vis. Sci. 2017;58(8):1758.
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© ARVO (1962-2015); The Authors (2016-present)
To determine the effect of primary blast exposure on retinal and optic nerve in an experimental shock-tube blast animal model.
Anesthetized adult male Long-Evan rats were placed in the target area of a compressed air-driven shock tube with their left sides facing the oncoming shock wave. Exposure groups experienced blast waves with peak overpressure of 123 ± 4 kPa and a positive phase duration of 3.34 ± 0.05 ms. The overpressure specific impulse was 148 ± 3 kPa-ms. Unexposed rats or shams were included as controls. The rats were euthanized while under anesthesia at 48 h post blast wave exposure. The retina and optic nerves tissues were subjected to immunohistochemistry, immunofluorescence, western and ELISA analysis for caspase-3, glial fibrillary acidic protein (GFAP), and aquaporin-4 (AQP4) expression, and TUNEL. Tissues were evaluated for relative levels of positive signals compared to unexposed controls.
Caspase-3 activation was observed in the retina and optic nerve of both the right and left eyes at 48 hour post blast exposure. However, a higher level of caspase-3 expression was observed in the left eye as compared to the contralateral eye and respective controls. Activated caspase-3 was detected preferentially in the inner nuclear layer and ganglion layer. GFAP was also expressed throughout the inner nuclear layer and ganglion layer. There was also increased AQP4 expression and retinal thickness on the left eye at 48 h post blast. In the optic nerve, the highest level in GFAP expression was detected on the left side and optic chiasm. A significant increase in TUNEL cells was observed through the retina and optic nerve preferentially in the left eye at 48 h post-injury.
Primary blast exposure resulted in retinal and optic nerve damage manifested by the increased expression of proteins involved in edema, gliosis, and apoptosis. The injury response was greater on the side facing the incident blast wave, and therefore subject to the reflected as well as the overpressure from blast wave. These findings support potential acute injury mechanisms in which increased water permeability, microglial activation, and apoptosis are caused by primary blast exposure. This experimental shock-tube blast animal model may be useful for analyzing the effect of therapeutic interventions on retinal damage due to primary blast waves.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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