モノクロタリン誘発肺高血圧症ラットモデルにおける水素吸入の肺炎症および血圧への影響
Using a monocrotaline-induced pulmonary hypertension model in male Wistar rats, this study examined the effects of continuous inhalation of atmospheric air containing 4% molecular hydrogen over 21 days. Monocrotaline was administered subcutaneously on day 1, and hemodynamic parameters were assessed under urethane anesthesia at day 21. Although hydrogen inhalation did not significantly alter the primary markers of pulmonary hypertension, systolic blood pressure was reduced in the hydrogen-exposed group. Additionally, TGF-β expression was decreased and the number of tryptase-containing mast cells in lung tissue was diminished. These findings suggest that hydrogen gas exerts partial anti-inflammatory and antioxidant effects in this oxidative stress-driven model, influencing systemic hemodynamics and inflammatory cell populations without fully reversing pulmonary vascular remodeling.
Molecular hydrogen selectively scavenges hydroxyl radicals, reducing oxidative stress induced by monocrotaline. This antioxidant action is associated with decreased TGF-β expression and a reduction in tryptase-positive mast cells, contributing to partial attenuation of lung inflammation and lowering of systolic blood pressure.
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/38137362