Distinguishing the Unique Neuropathological Profile of Blast Polytrauma

W. Brad Hubbard, Shaylen Greenberg, Carly Norris, Joseph Eck, Erin Lavik, Pamela Vandevord

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

Abstract

Traumatic brain injury sustained after blast exposure (blast-induced TBI) has recently been documented as a growing issue for military personnel. Incidence of injury to organs such as the lungs has decreased, though current epidemiology still causes a great public health burden. In addition, unprotected civilians sustain primary blast lung injury (PBLI) at alarming rates. Often, mild-to-moderate cases of PBLI are survivable with medical intervention, which creates a growing population of survivors of blast-induced polytrauma (BPT) with symptoms from blast-induced mild TBI (mTBI). Currently, there is a lack of preclinical models simulating BPT, which is crucial to identifying unique injury mechanisms of BPT and its management. To meet this need, our group characterized a rodent model of BPT and compared results to a blast-induced mTBI model. Open field (OF) performance trials were performed on rodents at 7 days after injury. Immunohistochemistry was performed to evaluate cellular outcome at day seven following BPT. Levels of reactive astrocytes (GFAP), apoptosis (cleaved caspase-3 expression), and vascular damage (SMI-71) were significantly elevated in BPT compared to blast-induced mTBI. Downstream markers of hypoxia (HIF-1α and VEGF) were higher only after BPT. This study highlights the need for unique therapeutics and prehospital management when handling BPT.

Original languageEnglish
Article number5175249
JournalOxidative Medicine and Cellular Longevity
Volume2017
DOIs
StatePublished - 2017

Bibliographical note

Publisher Copyright:
© 2017 W. Brad Hubbard et al.

ASJC Scopus subject areas

  • Biochemistry
  • Aging
  • Cell Biology

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