外傷性脳損傷後の急性肺損傷に対する水素吸入の効果：パイロトーシスおよびアポトーシスへの影響
Acute lung injury (ALI) secondary to traumatic brain injury (TBI) is a life-threatening condition in which inflammatory cascades and programmed cell death are central pathological drivers. Male Sprague-Dawley rats underwent fluid percussion injury and were subsequently exposed to 42% H2 (balanced with 21% O2 and nitrogen) for one hour daily. Animals in the TBI-only group exhibited marked pulmonary edema, elevated lung injury scores, and reduced oxygenation indices. Hydrogen inhalation significantly reduced pyroptosis-associated proteins—Caspase-1, ASC, and Gasdermin-D—alongside the pro-inflammatory cytokines IL-1β and IL-18. Apoptotic markers, including cleaved caspase-3 and the BCL-2/Bax ratio, were also favorably modulated. These findings indicate that high-concentration hydrogen inhalation accelerates endogenous recovery and attenuates both pyroptotic and apoptotic cell death pathways in TBI-induced ALI, suggesting potential utility in ICU settings.
Inhalation of 42% H2 suppresses pyroptosis by downregulating Caspase-1, ASC, and Gasdermin-D, while simultaneously reducing IL-1β and IL-18 levels and modulating cleaved caspase-3 and BCL-2/Bax to attenuate apoptotic cell death in lung tissue following TBI.
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.
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https://h2-papers.org/en/papers/34883075