クモ膜下出血後の早期脳損傷におけるラットへの水素ガス吸入による酸化ストレス軽減効果
This controlled animal study examined the effects of hydrogen gas inhalation on early brain injury in a rat subarachnoid hemorrhage (SAH) model induced by endovascular perforation. A total of 137 adult male Sprague-Dawley rats (280–350 g) received 2.9% H2 gas for 2 hours post-perforation. At 24 hours, H2 inhalation significantly reduced brain edema, attenuated blood-brain barrier disruption, decreased apoptosis, and improved neurological function. Oxidative damage markers—malondialdehyde (lipid), nitrotyrosine (protein), and 8-hydroxyguanosine (DNA)—were all reduced at 24 hours. However, these beneficial effects were not sustained at 72 hours. The findings indicate that the neuroprotective action of H2 in early SAH-related brain injury is primarily mediated through its antioxidative properties.
H2 gas scavenges reactive oxygen species, reducing oxidative damage to lipids (malondialdehyde), proteins (nitrotyrosine), and DNA (8-hydroxyguanosine), thereby suppressing apoptosis and preserving blood-brain barrier integrity to confer neuroprotection after SAH.
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/22336722