The aim of this study was to evaluate the neuroprotective efficacy of the inert gas
xenon as a treatment for patients with blast-induced
traumatic brain injury in an in vitro laboratory model. We developed a novel blast
traumatic brain injury model using C57BL/6N mouse organotypic hippocampal brain-slice cultures exposed to a single shockwave, with the resulting injury quantified using
propidium iodide fluorescence. A
shock tube blast generator was used to simulate open field
explosive blast shockwaves, modeled by the Friedlander waveform. Exposure to blast shockwave resulted in significant (p < 0.01) injury that increased with peak-overpressure and impulse of the shockwave, and which exhibited a secondary injury development up to 72 h after
trauma. Blast-induced
propidium iodide fluorescence overlapped with cleaved
caspase-3 immunofluorescence, indicating that
shock-wave-induced cell death involves apoptosis.
Xenon (50% atm) applied 1 h after blast exposure reduced injury 24 h (p < 0.01), 48 h (p < 0.05), and 72 h (p < 0.001) later, compared with untreated control injury.
Xenon-treated injured slices were not significantly different from uninjured
sham slices at 24 h and 72 h. We demonstrate for the first time that
xenon treatment after blast
traumatic brain injury reduces initial injury and prevents
subsequent injury development in vitro. Our findings support the idea that
xenon may be a potential first-line treatment for those with blast-induced
traumatic brain injury.