水素ガス吸入がマウス急性大動脈解離の増悪を抑制する
Acute aortic dissection (AAD) is a life-threatening vascular condition in which inflammatory processes drive disease progression and complications including rupture. Using a murine AAD model established by β-aminopropionitrile pretreatment combined with continuous angiotensin II infusion, male C57BL/6J mice were exposed to 2% H2 gas or control gas for 24 hours. H2 inhalation improved 24-hour survival and spontaneous locomotor activity without altering systolic blood pressure. Aortic rupture frequency and false lumen expansion were both reduced. Plasma IL-6 and G-CSF concentrations declined significantly, and MMP-9 and CXCL1 showed decreasing trends. Within the aortic wall, MMP-9 and CXCL1 expression—particularly in Ly-6B.2-positive regions—was diminished, and the number of Ly-6B.2-positive cells correlated positively with false lumen area. In bone marrow, the AAD-associated reduction in CD11b+Ly-6G+ neutrophils was significantly attenuated by H2 inhalation. Oxidative stress markers in the aortic wall were also reduced. These results suggest that 2% H2 gas inhalation limits AAD exacerbation through modulation of neutrophil-mediated inflammation and oxidative stress.
H2 inhalation reduces circulating IL-6 and G-CSF, suppresses MMP-9 and CXCL1 expression in the aortic wall, decreases neutrophil (Ly-6B.2-positive cell) infiltration, and attenuates oxidative stress, collectively limiting false lumen expansion and aortic rupture in AAD.
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/42105975