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Exposure of swine to nonpenetrating blast results in reactive astrogliosis, fiber degeneration, and upregulation of inflammatory markers
Author(s) -
Tong Lawrence,
Januszkiewicz Adolph J,
Swauger Peter V,
Lanerolle Nihal C,
Kim Jung H,
Gyorgy Andrea B,
Agoston Denes V,
Bandak Faris A,
Ling Geoffrey S,
Parks Steven A
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.926.1
Subject(s) - astrogliosis , traumatic brain injury , medicine , cerebrospinal fluid , neuroscience , pathology , hippocampus , blast injury , degeneration (medical) , biology , poison control , central nervous system , environmental health , psychiatry
Blast‐induced nonpenetrating brain injury (bTBI) has become increasingly prevalent in recent years. The arsenal of available treatments continues to be inadequate while the mechanism of injury remains equivocal. Although similar studies have been reported on small animal models using fluid percussion and weight‐driven devices, none have been conducted on large animals under real‐world conditions. We exposed swine to varying levels of focused explosions within a shock tube in order to quantify the intensities needed to produce minimum detectable and maximum survivable bTBI. In addition, improvised explosive devices were detonated near swine placed within a surrogate Humvee, in a simulated building/street setting, or in an open‐field scenario. All animals were exposed left‐laterally to incident explosion. Early histological findings are distinctly different from other causes of TBI and include activation of astrocytes in the hippocampus and overlapping fiber tracts as well as fiber degeneration in the thalamus and anterior cerebellar vermis, that do not clearly correlate with exposure lateralization. Preliminary proteomic analyses of cerebrospinal fluid, blood and brain tissue indicate blood‐brain barrier disruption along with a prominent inflammatory response.