ラットモデルにおける心停止後症候群に対する水素ガス吸入の効果：治療的低体温法との比較
Using a rat ventricular fibrillation model, this study examined the effects of 2% H2 gas inhalation initiated at the start of cardiopulmonary resuscitation on post-cardiac arrest syndrome. Four groups were compared: normothermia with N2, normothermia with H2, therapeutic hypothermia (TH, 33°C) with N2, and TH with H2. Gas mixtures and TH were maintained for 2 hours after return of spontaneous circulation. H2 inhalation improved survival rates and neurological deficit scores to a degree comparable to TH. Unlike TH, H2 inhalation also prevented increases in left ventricular end-diastolic pressure and serum IL-6 levels. Marked reductions in 8-OHdG- and 4-HNE-positive cardiomyocytes indicated that hydroxyl radical scavenging contributed substantially to these protective effects. Combined H2 inhalation and TH did not produce additive benefits beyond either intervention alone.
H2 gas scavenges hydroxyl radicals, thereby reducing oxidative DNA damage (8-OHdG) and lipid peroxidation (4-HNE) in cardiomyocytes and attenuating ischemia-reperfusion injury following cardiac arrest.
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/23316300