Effects of hypobaric hypoxia during a simulated ultra-long-haul flight on inflammation and regeneration after muscle trauma and muscle trauma-hemorrhagic shock.

Abstract

Because wounded warfighters or trauma victims may receive en route care to the closest medical facility via airplane transport, we investigated the effects of extended mild hypobaric hypoxia (HB), the environmental milieu of most airplanes, on inflammation and regeneration after muscle trauma or monotrauma (MT) and muscle trauma-hemorrhagic shock or polytrauma (PT). Male C57BL/6N mice were assigned to one of six groups pertaining to injury (control/uninjured, MT, and PT) and atmospheric pressure exposure (HB and normobaric normoxia, NB). Body mass, blood and muscle leukocyte number by flow cytometry, immunohistochemistry, or both, and the muscle relative mRNA level of selected genes involved in inflammation and muscle regeneration were examined at ~1.7, 4, 8, and 14 days post trauma (dpt). At 14 dpt, the proportion of smaller- and larger-sized myofibers at the regenerating site of MT mice was determined. Greater body mass loss, an increased number of blood and muscle leukocytes, and differential muscle relative mRNA levels were observed in MT and PT groups compared to controls. The MT+HB or PT+HB mice demonstrated more body mass loss and altered relative mRNA level than the corresponding NB mice. Additionally, a subgroup of MT+HB mice demonstrated a greater proportion of smaller myofibers (250 to 500 μm2 ) than MT+NB mice at 14 dpt. HB exposure after muscle trauma alone may prolong regeneration. Following HB exposure, therapies that promote oxygenation may be needed during this muscle recovery.