Purchase this article with an account.
Jessica Hines-Beard, Jeffrey Marchetta, Edward Chaum, Sarah Gordon, Eldon E. Geisert, Tonia S. Rex; Novel Ocular Blast Injury Model. Invest. Ophthalmol. Vis. Sci. 2012;53(14):4974. doi: https://doi.org/.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
We have developed a mouse model of primary ocular blast injury.
A modified paintball gun was used to deliver short blasts of compressed air. The gun has a pressure output regulator for tightly controlled and adjustable pressure output. A pressure transducer is used to measure the pressure delivered to the eye through a small opening in a housing module. Three-month-old C57/Bl6 mice were exposed to a single blast to the left eye only, contralateral eyes served as internal controls. Before- and immediately post-blast, intraocular pressure (IOP) and gross pathology were recorded for both eyes. IOP, gross pathology, optical coherence tomography (OCT), and optokinetics were performed at 3, 7, 14, and 28 days post-blast.
The blast system generates a waveform that models an open-field blast. After exposure to a 26psi blast, corneal abrasions and edema were seen in a small minority of mice that resolved by 28 days post-blast. Other findings included corneal neovascularization, pupillary sphincter tear, cataract and hyphema. Higher blast exposures resulted in extraocular muscle tears and avulsion of the optic nerve in 25% of mice. No increase in IOP was detected post-blast. A large area of damage to the peripheral outer retina was detected by OCT after exposure to a 26psi blast. Blast exposure had no effect on visual acuity until 28 days after exposure to a 30psi blast.
Our novel model of primary ocular blast injury successfully and reproducibly induced both anterior segment and retinal injuries in the eye. This model can be used to test the molecular mechanisms of blast injury responses in the eye and the efficacy of different treatments.
This PDF is available to Subscribers Only