Abstract SNACC-56

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Aeromedical Evacuation-Relevant Hypobaria Worsens Axonal Injury and Blood Brain Barrier Disruption Induced by Underbody Blast-induced Hyperacceleration

1Proctor J, 2Fourney W, 1Puche A, 1Faden A, 1Rosenthal R, 1Fang R, 1Rangghran P, 1Fiskum G
1university of maryland, Baltimore, Maryland, United states; 2University of Maryland, college park, Maryland, United states

Introduction
Occupants of vehicles targeted by buried IEDs often sustain TBI. Warfighters that experience underbody blasts are aerially evacuated (AE) to a regional military medical center usually within a few days after injury. This study tested the hypothesis that exposure of rats to AE-relevant hypobaria worsens TBI caused by underbody blasts.
Methods
The underbody blast device consists of a water tank in which a platform is located that supports a thick aluminum plate located above the water line. The plate can travel vertically, guided by poles located in holes in each corner of the plate. The two cylinders secured to the top of the plate each house a ketamine-anesthetized, immobilized male rat. An explosive charge is placed in the water precisely under the center of the plate at various stand-off distances that generate peak G-forces of from 100 - 700 Gs within 2 msec after the explosion. At 7 days after the blast, rats were perfusion-fixed and their brains analyzed for evidence of axonal fiber injury (de Olmos silver staining), and cerebrovascular injury (IgG for blood brain permeability (BBB) disruption). Quantification of silver-stained axons and number of IgG effusions employed a stereologic approach and StereoInvestigator software.
Results
The number of silver-stained axonal fibers (line crossings per 5000 μm2) in the internal capsule was significantly greater in animals (n = 10/group) exposed to 100 G blast than in shams (8,0 ± 1.2 vs 3.9 ± 1.0), and three-times greater following 700 G blasts (12.5 ± 1.3). Animals exposed to 6 hr hypobaria (= 8000 ft altitude) at 6, 24, or 72 hr after the 100 G blasts all exhibited significantly more silver-stained fibers than those not exposed to hypobaria (14.7 ± 0.9; 19.8 ± 1.4; 15.3 ± 1.2, respectively). The number of perivascular IgG effusions present in the hippocampus (per mm2) was also greater in animals (n=5/group) exposed to either 100 or 700 Gs (7.2 ± 1.4; 21.2 ± 3.9), compared to shams (3.0 ± 0.8). Preliminary results also suggest that exposure to hypobaria at 24 hr following exposure to 100 Gs blasts further increases the number of hippocampal IgG effusions (30.4 ± 5.7).
Conclusions
1. Underbody blast-induced acceleration loads of 100 – 700 Gs produce region-selective axonopathy quantifiable by silver staining. 2. BBB disruption occurs in the hippocampus after exposure of rats to blast-induced high G-forces. 3. Exposure to hypobaria similar to that experienced during AE causes an increase in axonopathy and blood brain barrier disruption. 4. These results represent the first quantitative evidence that blast-induced acceleration alone, in the absence of exposure to blast overpressure, results in white matter and cerebrovascular injury. 5. The increase in injury caused by exposure to AE-relevant hypobaria raises concerns about when it is safe-to-fly warfighters with TBIs. Further studies will determine the minimum delay before AE that is necessary to avoid exacerbation of different forms of brain injury.
Acknowledgments
Support from US Air Force Medical Service FA8650-11-2-6D04 and US Dept. of Defense W81-xWH-13-1-0016


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