吸入水素によるポストコンディショニングがラット網膜虚血再灌流傷害モデルにおける網膜神経節細胞の生存を促進する
Using a rat model of retinal ischemia/reperfusion (I/R) injury, this study examined whether postconditioning with high-concentration inhaled hydrogen (67% H2 / 33% O2, 1 hour daily for 7 days beginning immediately after ischemia) could protect retinal ganglion cells (RGCs). RGC density assessed by hematoxylin-eosin staining and retrograde cholera toxin beta labeling was significantly greater in hydrogen-treated animals than in untreated I/R controls. Visual function measured by flash visual evoked potentials and pupillary light reflex was also better preserved in the hydrogen group. Oxidative stress marker 4-hydroxynonenal (4-HNE)-positive cell counts in the ganglion cell layer were reduced, and retinal overexpression of IL-1β and TNF-α induced by I/R was suppressed. These findings indicate that inhaled hydrogen postconditioning confers neuroprotection against retinal I/R injury through concurrent suppression of oxidative stress, inflammatory signaling, and apoptotic pathways.
Inhalation of 67% H2 reduces 4-hydroxynonenal accumulation and suppresses I/R-induced overexpression of IL-1β and TNF-α, thereby protecting retinal ganglion cells via coordinated inhibition of oxidative stress, inflammatory, and apoptotic pathways.
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/26705611