Hypobaric hypoxia exacerbates the neuroinflammatory response to traumatic brain injury. J Surg Res 2011 Jan;165(1):30-7
Date
09/21/2010Pubmed ID
20850781Pubmed Central ID
PMC4607063DOI
10.1016/j.jss.2010.05.055Scopus ID
2-s2.0-78649962095 (requires institutional sign-in at Scopus site) 53 CitationsAbstract
OBJECTIVE: To determine the inflammatory effects of time-dependent exposure to the hypobaric environment of simulated aeromedical evacuation following traumatic brain injury (TBI).
METHODS: Mice were subjected to a blunt TBI or sham injury. Righting reflex response (RRR) time was assessed as an indicator of neurologic recovery. Three or 24 h (Early and Delayed groups, respectively) after TBI, mice were exposed to hypobaric flight conditions (Fly) or ground-level control (No Fly) for 5 h. Arterial blood gas samples were obtained from all groups during simulated flight. Serum and cortical brain samples were analyzed for inflammatory cytokines after flight. Neuron specific enolase (NSE) was measured as a serum biomarker of TBI severity.
RESULTS: TBI resulted in prolonged RRR time compared with sham injury. After TBI alone, serum levels of interleukin-6 (IL-6) and keratinocyte-derived chemokine (KC) were increased by 6 h post-injury. Simulated flight significantly reduced arterial oxygen saturation levels in the Fly group. Post-injury altitude exposure increased cerebral levels of IL-6 and macrophage inflammatory protein-1α (MIP-1α), as well as serum NSE in the Early but not Delayed Flight group compared to ground-level controls.
CONCLUSIONS: The hypobaric environment of aeromedical evacuation results in significant hypoxia. Early, but not delayed, exposure to a hypobaric environment following TBI increases the neuroinflammatory response to injury and the severity of secondary brain injury. Optimization of the post-injury time to fly using serum cytokine and biomarker levels may reduce the potential secondary cerebral injury induced by aeromedical evacuation.
Author List
Goodman MD, Makley AT, Huber NL, Clarke CN, Friend LA, Schuster RM, Bailey SR, Barnes SL, Dorlac WC, Johannigman JA, Lentsch AB, Pritts TAAuthor
Callisia N. Clarke MD Chief, Associate Professor in the Surgery department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBrain Injuries
Chemokine CCL3
Hypoxia
Inflammation
Interleukin-6
Male
Mice
Mice, Inbred C57BL
Phosphopyruvate Hydratase
Reflex, Righting
