慢性的な水素ガス吸入による敗血症関連の短期・長期記憶障害の軽減
Sepsis rapidly affects the central nervous system through circulating inflammatory mediators that penetrate the hippocampus and prefrontal cortex, inducing neuroinflammation and subsequent memory deficits. Using a polymicrobial sepsis animal model, this study examined whether chronic molecular hydrogen inhalation could mitigate both short- and long-term memory impairment. Behavioral assessments demonstrated that chronic H2 exposure reduced sepsis-associated memory loss. Additionally, acute H2 inhalation lowered neuroinflammatory markers in memory-relevant brain regions and elevated total Nrf2 protein levels—a transcription factor governing a broad array of antioxidant and anti-inflammatory gene expressions. These findings suggest that H2 inhalation may represent a feasible and safe approach to limiting sepsis-induced cognitive deterioration.
H2 inhalation suppresses neuroinflammation in the hippocampus and prefrontal cortex while upregulating total Nrf2 protein, thereby modulating antioxidant and anti-inflammatory gene expression and attenuating sepsis-induced memory deficits.
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/32348775