高圧水素吸入による外傷性脳損傷後の二次性脳障害への影響：マウスモデルを用いた検討
Secondary brain injury following traumatic brain injury (TBI) involves biochemical cascades driven largely by oxidative stress, making molecular hydrogen a candidate intervention. In this mouse study, 120 animals were allocated to three groups: TBI without intervention, TBI with hyperbaric hydrogen (HBH2) at 2 atmospheres for 90 minutes beginning 30 minutes post-injury, and a sham group. Moderate cerebral contusion was induced via controlled cortical impact. Compared with the untreated TBI group, the HBH2 group exhibited significantly reduced cerebral edema, a greater number of surviving hippocampal neurons at day 28, and markedly lower hyperactivity scores at day 14. These findings suggest that elevating hydrogen partial pressure through hyperbaric conditions enhances neuroprotective efficacy beyond what atmospheric-pressure delivery can achieve.
Increasing ambient pressure raises hydrogen partial pressure, enabling greater reactive oxygen species scavenging that attenuates oxidative-stress-driven secondary injury, thereby reducing cerebral edema and preserving hippocampal neurons.
For inhalation applications of molecular hydrogen, the lower flammability limit (LFL) deserves careful handling. The classical 4% figure applies to closed-system mixtures; the practical inhalation-environment threshold is 10%. Even pure-hydrogen output (the UFL 75% paradox) passes through the flammable range at the air–gas boundary. High-concentration (66% / 100%) inhalers are documented in the Japanese Consumer Affairs Agency accident-information database and are not recommended.
See also:
https://h2-papers.org/en/papers/38055881