マウス両側総頸動脈閉塞モデルにおける水素ガス吸入の効果
Male C57BL/6J mice underwent transient bilateral common carotid artery occlusion (BCCAO) using a nontraumatic aneurysm clip and were assigned to sham, BCCAO, or BCCAO plus 1.3% hydrogen gas inhalation groups. Cerebral blood flow in both cortical hemispheres was monitored continuously via laser Doppler perfusion imaging, and vital signs were recorded throughout. At 24 hours post-ischemia, oxidative stress was quantified by 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels, neuronal damage in the hippocampal CA1 region was histologically assessed, and brain water content was measured. Hydrogen gas administration did not alter vital signs or cerebral blood flow. Nevertheless, 8-OHdG expression was reduced, hippocampal CA1 neuronal injury was diminished, and brain edema was attenuated in hydrogen-treated animals, suggesting a neuroprotective role for hydrogen gas in this ischemia model.
Hydrogen gas is proposed to selectively scavenge hydroxyl radicals, thereby reducing oxidative DNA damage (8-OHdG), attenuating hippocampal CA1 neuronal injury, and limiting cerebral edema following bilateral carotid occlusion.
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/23564105