2%水素吸入による熱中症ラットの生存率改善と血管内皮グリコカリックス脱落抑制効果
Heat stroke induces severe oxidative stress and systemic inflammation, contributing to vascular endothelial glycocalyx shedding and elevated mortality. This animal study used 98 Wistar rats exposed to a 40°C, 60% humidity chamber to model heat stroke, followed by inhalation of 0%, 2%, or 4% hydrogen gas for one hour. Survival rates, glycocalyx thickness in the left ventricle, and multiple serum biomarkers were assessed. Rats receiving 2% hydrogen showed significantly improved survival and partial preservation of glycocalyx thickness. Serum concentrations of endotoxin, syndecan-1, malondialdehyde, and tumor necrosis factor-α were reduced, while superoxide dismutase activity increased. These findings indicate that 2% hydrogen inhalation confers protection against glycocalyx degradation through antioxidative and anti-inflammatory mechanisms. The 4% concentration did not demonstrate equivalent benefit, suggesting a dose-dependent response.
Inhalation of 2% H2 suppresses oxidative stress (reduced malondialdehyde) and inflammatory signaling (reduced TNF-α) while enhancing superoxide dismutase activity, collectively limiting enzymatic and oxidative degradation of the vascular endothelial glycocalyx.
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/34524269