• Julie L Proctor, Kaitlin T Mello, Raymond Fang, Adam C Puche, Robert E Rosenthal, William L Fourney, Ulrich H Leiste, and Gary Fiskum.
• From the Department of Anesthesiology (J.L.P., K.T.M., GF.), University of Maryland School of Medicine, Program in Trauma (R.F., R.E.R.), R. Adams Cowley Shock Trauma Center, University of Maryland Medical Center; U.S. Air Force Center for the Sustainment of Trauma and Readiness Skills (R.F.); Department of Anatomy and Neurobiology (A.C.P.), Department of Emergency Medicine (R.E.R.), University of Maryland School of Medicine, Baltimore; and School of Engineering (W.L.F., U.L.H.), University of Maryland College Park, College Park, Maryland.
• J Trauma Acute Care Surg. 2017 Jul 1; 83 (1 Suppl 1): S35-S42.

BackgroundOccupants of military vehicles targeted by explosive devices often suffer from traumatic brain injury (TBI) and are typically transported by the aeromedical evacuation (AE) system to a military medical center within a few days. This study tested the hypothesis that exposure of rats to AE-relevant hypobaria worsens cerebral axonal injury and neurologic impairment caused by underbody blasts.MethodsAnesthetized adult male rats were secured within cylinders attached to a metal plate, simulating the hull of an armored vehicle. An explosive located under the plate was detonated, resulting in a peak vertical acceleration force on the plate and occupant rats of 100G. Rats remained under normobaria or were exposed to hypobaria equal to 8,000 feet in an altitude chamber for 6 hours, starting at 6 hours to 6 days after blast. At 7 days, rats were tested for vestibulomotor function using the balance beam walking task and euthanized by perfusion. The brains were then analyzed for axonal fiber injury.ResultsThe number of internal capsule silver-stained axonal fibers was greater in animals exposed to 100G blast than in shams. Animals exposed to hypobaria starting at 6 hours to 6 days after blast exhibited more silver-stained fibers than those not exposed to hypobaria. Rats exposed to 100% oxygen (O2) during hypobaria at 24 hours postblast displayed greater silver staining and more balance beam foot-faults, in comparison with rats exposed to hypobaria under 21% O2.ConclusionExposure of rats to blast-induced acceleration of 100G increases cerebral axonal injury, which is significantly exacerbated by exposure to hypobaria as early as 6 hours and as late as 6 days postblast. Rats exposed to underbody blasts and then to hypobaria under 100% O2 exhibit increased axonal damage and impaired motor function compared to those subjected to blast and hypobaria under 21% O2. These findings raise concern about the effects of AE-related hypobaria on TBI victims, the timing of AE after TBI, and whether these effects can be mitigated by supplemental oxygen.

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