ウサギ脊髄虚血再灌流障害に対する水素ガス吸入の保護効果
A rabbit model of spinal cord ischemia was established by occluding the infrarenal aorta for 20 minutes in male New Zealand white rabbits. Hydrogen gas at concentrations of 1%, 2%, or 4% was administered by inhalation beginning 10 minutes before reperfusion and continuing for 60 minutes afterward (70 minutes total). Animals receiving 2% or 4% H2 showed significant preservation of normal motor neuron counts and improved hindlimb motor function compared with untreated controls. Biochemical analyses of serum and spinal cord tissue revealed reductions in oxidative stress markers (8-iso-PGF2α and MDA) and pro-inflammatory cytokines (TNF-α and HMGB1), alongside elevated activities of antioxidant enzymes (SOD and catalase). Motor neuron apoptosis in the spinal cord was also markedly reduced in H2-treated animals, suggesting that hydrogen inhalation engages antioxidant and anti-inflammatory pathways to confer neuroprotection following spinal cord ischemia-reperfusion.
H2 inhalation reduces lipid peroxidation products (8-iso-PGF2α, MDA) and pro-inflammatory cytokines (TNF-α, HMGB1) while enhancing SOD and catalase activities, thereby suppressing oxidative damage and motor neuron apoptosis in ischemia-reperfusion-injured spinal cord tissue.
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/21195696