Hydrogen Gas Inhalation Prevents Dangerous Aortic Tears in Mice

Authors
Journal
Life Sciences
Year
DOI
10.1016/j.lfs.2026.124443
Study Type
Mouse
Outcome
Positive
Peer Reviewed
Yes
Country
Japan
Health Condition
Acute Aortic Dissection
Body System
Cardiovascular

TL;DR

In a mouse model of acute aortic dissection, 2% hydrogen gas inhalation improved short-term survival, reduced aortic rupture and false lumen expansion, and dampened neutrophil-associated inflammation without lowering blood pressure.

Key Finding

Inhaled hydrogen gas reduced aortic rupture frequency and improved survival in mice with acute aortic dissection by suppressing inflammatory markers and neutrophil activity, without affecting blood pressure.

Summary

This study tested whether inhaled hydrogen gas could help protect mice from acute aortic dissection, a life-threatening condition where the main artery tears and becomes inflamed. Researchers induced this condition in mice and exposed some to 2% hydrogen gas for 24 hours. Mice that inhaled hydrogen gas had better survival rates, less aortic rupture, and showed reduced levels of inflammatory molecules (immune signals that cause tissue damage) compared to control mice, without any changes in blood pressure.

Practical Takeaway

This is early-stage research conducted only in mice, so it cannot yet be applied to human health. The findings suggest hydrogen gas inhalation may warrant further investigation as a potential supportive therapy for aortic dissection, but human studies would be needed to determine if these protective effects translate to people and whether the approach is safe and practical in a clinical setting.

Abstract

Aims: Acute aortic dissection (AAD) is a life-threatening condition in which vascular inflammation contributes to disease progression and complications such as aortic rupture. Current treatment is centered on hemodynamic control, and anti-inflammatory options remain limited. We investigated whether inhaled molecular hydrogen (H2) gas attenuates AAD severity in a murine model. Materials and methods: AAD was induced in male C57BL/6J mice by β-aminopropionitrile pretreatment followed by continuous angiotensin II infusion. Mice were exposed to 2% H2 gas or control gas for 24 h, and effects on AAD severity and inflammation were examined. Key findings: H2 inhalation improved 24-h survival and spontaneous locomotor activity, while systolic blood pressure was not altered. H2 also reduced aortic rupture frequency and suppressed false lumen enlargement. In plasma, H2 inhalation significantly reduced IL-6 and G-CSF levels, while MMP-9 and CXCL1 showed downward trends. In the aortic wall, H2 reduced MMP-9 and CXCL1 expression, including within Ly-6B.2-positive regions, whereas CXCL1 expression within SMA-positive regions was unchanged. In addition, the number of Ly-6B.2-positive cells in the aortic wall was decreased and positively correlated with false lumen area. In bone marrow, the reduction in CD11b+Ly-6G+ neutrophils observed in AAD mice was significantly attenuated by H2 inhalation. H2 also attenuated oxidative stress-related changes in the aortic wall. Significance: These findings indicate that 2% H2 gas inhalation reduces acute AAD exacerbation without affecting blood pressure, likely through modulation of inflammatory mediators and neutrophil-associated acute inflammation. H2 inhalation may represent a safe adjunctive strategy to limit AAD progression and rupture.