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Elaine Por, Jae-Hyek Choi, Brian J Lund; Low-level blast exposure increases Transient Receptor Potential Vanilloid 1 (TRPV1) expression in the rat cornea. Invest. Ophthalmol. Vis. Sci. 2016;57(12):5724.
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© ARVO (1962-2015); The Authors (2016-present)
Blast-related ocular injuries sustained by military personnel have led to rigorous efforts to elucidate the effects of blast exposure on neurosensory function. Recent studies have provided some insight on cognitive and visual deficits sustained following blast exposure; however limited data is available on the effects of low-level blast on pain and inflammatory processes. Investigation of these secondary effects of blast exposure is necessary to fully comprehend the complex pathophysiology of blast-related injuries. The overall purpose of this study is to determine the effects of single and repeated low-level blast exposure on pain and inflammatory mediators in ocular sensory tissues.
A compressed air shock tube was used to deliver a single or repeated blast (68.0 ± 2.7 kPa) to anesthetized rats daily for five consecutive days. Immunohistochemistry was performed on ocular tissues to determine expression of the Transient Receptor Potential Vanilloid 1 (TRPV1) channel, calcitonin gene related peptide (CGRP), substance P (SP) and endothelin-1 (ET-1) following single and repeated blast exposure. Neutrophil infiltration and myeloperoxidase (MPO) expression were also assessed in blast tissues via immunohistochemistry and ELISA analysis, respectively.
TRPV1 expression was increased in rat corneas exposed to both single and repeated low-level blast. Increased secretion of CGRP, SP, and ET-1 was also detected in rat corneas as compared to control. Repeated blast exposure resulted in neutrophil infiltration in the cornea and stromal layer. Moreover, increased levels of blood myeloperoxidase (MPO), a peroxidase enzyme abundantly expressed in the azurophilic granules of neutrophils, was detected in rats following repeated blast suggesting a cumulative effect of low-level blast.
Single and repeated low-level blast exposure resulted in increased expression of TRPV1, CGRP, SP and ET-1 in the rat cornea. Increased neutrophil infiltration and plasma MPO expression following blast exposure demonstrated activation of inflammatory mechanisms. Collectively, these findings provide novel insight into the activation of pain and inflammation signaling mediators following blast exposure.
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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