水素ガス吸入による術後認知機能障害の軽減：ラットモデルを用いた検討
Using a rat tibial fracture surgery model under anesthesia, this study examined whether 2% H2 inhalation for 3 hours (starting 1 hour post-surgery) could mitigate postoperative cognitive dysfunction. Cognitive assessments via fear conditioning and Y-maze tests on days 1, 3, and 7 revealed significant impairment in surgery-only animals, which was substantially reversed by H2 inhalation. Biochemical analyses showed that H2 suppressed elevated levels of proinflammatory cytokines—TNF-α, IL-1β, IL-6, and HMGB1—in both serum and hippocampal tissue. Additionally, blood-brain barrier integrity was better preserved and hippocampal caspase-3 activity was reduced in H2-treated animals. The findings indicate that modulation of inflammatory signaling and apoptotic pathways underlies the neuroprotective effects of inhaled H2 in this surgical context.
Inhaled H2 suppresses proinflammatory cytokines (TNF-α, IL-1β, IL-6, HMGB1) in serum and hippocampus, reduces caspase-3-mediated apoptosis, and preserves blood-brain barrier integrity, collectively attenuating surgery-induced cognitive decline.
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/28614179