心不全早期における分子状水素吸入の微小循環・代謝・酸化ストレス・心筋状態への影響
Using a rat model of chronic heart failure (CHF) induced by catecholamine administration, this study investigated the impact of H2 gas inhalation administered either as a single 40-minute session or repeatedly over five consecutive days (40 minutes daily). Microcirculatory parameters were assessed via laser Doppler flowmetry and laser fluorescence spectroscopy, while lipid peroxidation was quantified in both plasma and myocardial tissue, and histological examination was conducted. Single and repeated H2 inhalation both improved microvascular perfusion (p < 0.05), with restoration of central regulatory mechanisms and activation of local vascular control—changes that contrasted with the impaired perfusion seen in untreated CHF animals. Oxidative stress markers and metabolic disturbances were reduced more substantially following multiple administrations. Histological data indicated that repeated H2 exposure decreased myocardial edema and helped maintain tissue architecture during cardiac remodeling, suggesting a protective role in early CHF progression.
H2 inhalation activates local microvascular regulation and restores central hemodynamic control, while suppressing lipid peroxidation in plasma and myocardium, thereby reducing myocardial edema and limiting tissue remodeling in early heart failure.
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/41462618