敗血症に対する水素ガスの有望な効果：酸化ストレス・炎症・アポトーシス調節機序のレビュー
Sepsis, defined by a systemic inflammatory response to infection, continues to impose substantial morbidity and mortality in critically ill populations despite advances in critical care. This review consolidates findings on molecular hydrogen (H2) gas in experimental sepsis models. Studies using cecal ligation and puncture (CLP), zymosan, and lipopolysaccharide (LPS) induction in mice and rats demonstrated that H2 gas improved survival rates and reduced organ damage. The underlying mechanisms appear to involve suppression of oxidative stress, modulation of inflammatory cascades, and regulation of apoptotic pathways, potentially mediated through NF-κB and Nrf2/HO-1 signaling. The authors summarize the current state of evidence for H2 in sepsis research.
H2 gas modulates oxidative stress, inflammatory responses, and apoptosis via NF-κB and Nrf2/HO-1 signaling pathways, thereby reducing organ damage and improving survival in rodent sepsis models.
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/24829918