Air-Evacuation-Relevant Hypobaria Following Traumatic Brain Injury Plus Hemorrhagic Shock in Rats Increases Mortality and Injury to the Gut, Lungs, and Kidneys

Abstract

Rats exposed to hypobaria equivalent to what occurs during aeromedical evacuation within a few days after isolated traumatic brain injury exhibit greater neurologic injury than those remaining at sea level. Moreover, administration of excessive supplemental O₂ during hypobaria further exacerbates brain injury. This study tested the hypothesis that exposure of rats to hypobaria following controlled cortical impact (CCI)-induced brain injury plus mild hemorrhagic shock worsens multiple organ inflammation and associated mortality. In this study, at 24 hr after CCI plus hemorrhagic shock, rats were exposed to either normobaria (sea level) or hypobaria (=8000 ft altitude) for 6 hr under normoxic or hyperoxic conditions. Injured rats exhibited mortality ranging from 30% for those maintained under normobaria and normoxia to 60% for those exposed to 6 hr under hypobaric and hyperoxia. Lung histopathology and neutrophil infiltration at 2 days post injury were exacerbated by hypobaria and hyperoxia. Gut and kidney inflammation at 30 days post-injury were also worsened by hypobaric hyperoxia. In conclusion, exposure of rats after brain injury and hemorrhagic shock to hypobaria or hyperoxia results in increased mortality. Based on gut, lung, and kidney histopathology at 2–30 days post-injury, increased mortality is consistent with multi-organ inflammation. These findings support epidemiological studies indicating that increasing aircraft cabin pressures to 4000 ft altitude (compared to standard 8000 ft.) and limiting excessive oxygen administration will decrease critical complications during and following aeromedical transport.