Hydrogen Gas Inhalation Attenuates Acute Impulse Noise Trauma: A Preclinical In Vivo Study.

Objective: Molecular hydrogen (H ₂ ) has shown therapeutic potential in several oxidative stress-related conditions in humans, is well-tolerated, and is easily administered via inhalation.The aim of this preclinical in vivo study was to investigate whether impulse noise trauma can be prevented by H ₂ when inhaled immediately after impulse noise exposure.
Methods: Guinea pigs (n = 26) were subjected to impulse noise (n = 400; 156 dB SPL; 0.33/s; n = 11; the Noise group), to impulse noise immediately followed by H ₂ inhalation (2 mol%; 500 ml/min; 1 hour; n = 10; the Noise + H ₂ group), or to H ₂ inhalation (n = 5; the H ₂ group). The acoustically evoked ABR threshold at 3.15, 6.30, 12.5, 20.0, and 30.0 kHz was assessed before and 4 days after impulse noise and/or H ₂ exposure. The cochleae were harvested after the final ABR assessment for quantification of hair cells.
Results: Noise exposure caused ABR threshold elevations at all frequencies (median 35, 35, 30, 35, and 35 dB SPL, the Noise group; 20, 25, 10, 13, and 20 dB SPL, the Noise + H ₂ group; P  < .05) but significantly less so in the Noise + H ₂ group ( P  < .05). Outer hair cell (OHC) loss was in the apical, mid, and basal regions 8.8%, 53%, and 14% in the Noise group and 3.5%, 22%, and 1.2% in the Noise + H ₂ group. The corresponding inner hair cell (IHC) loss was 0.1%, 14%, and 3.5% in the Noise group and 0%, 2.8%, and 0% in the Noise + H ₂ group. The difference between the groups was significant in the basal region for OHCs ( P  = .003) and apical ( P  = .033) and basal ( P  = .048) regions for IHCs.
Conclusions: Acute acoustic trauma can be reduced by H ₂ when inhaled immediately after impulse noise exposure.