Hydrogen Gas Inhalation Improves Survival in Severe Blood Loss Shock
- Authors
- Tomoyoshi Tamura, Motoaki Sano, Tadashi Matsuoka, Joe Yoshizawa, Ryo Yamamoto, Yoshinori Katsumata, Jin Endo, Koichiro Homma, Mayumi Kajimura, Masaru Suzuki, Eiji Kobayashi, Junichi Sasaki
- Journal
- Shock
- Year
- 2020
- DOI
- 10.1097/SHK.0000000000001459
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Hemorrhagic Shock
- Body System
- Cardiovascular
TL;DR
Breathing in hydrogen gas helps rats recover from severe blood loss by stabilizing their blood pressure and increasing their chances of survival, partly by reducing inflammation and protecting blood vessel linings.
Key Finding
Hydrogen gas inhalation stabilized blood pressure and improved survival rates in rats experiencing severe hemorrhagic shock, working through a mechanism that reduces inflammation rather than through the xanthine oxidoreductase pathway.
Summary
This study tested whether hydrogen gas inhalation could help rats survive severe blood loss and shock. Researchers induced shock in rats, then gave them either regular oxygen or oxygen mixed with hydrogen gas to breathe. They found that hydrogen gas helped stabilize blood pressure and improved survival rates. The study suggests hydrogen works by reducing inflammation and protecting the inner lining of blood vessels (called the endothelial glycocalyx), which is damaged during shock.
Practical Takeaway
This is early-stage research conducted only in rats, so it cannot yet be applied to human health. While the findings suggest hydrogen gas may have protective effects during severe shock, much more research—including human studies—would be needed before any clinical applications could be considered. The study does not address hydrogen water consumption, only direct hydrogen gas inhalation in a medical emergency setting.
Abstract
Background: Hydrogen gas (H2) inhalation during hemorrhage stabilizes post-resuscitation hemodynamics, improving short-term survival in a rat hemorrhagic shock and resuscitation (HS/R) model. However, the underlying molecular mechanism of H2 in HS/R is unclear. Endothelial glycocalyx (EG) damage causes hemodynamic failure associated with HS/R. In this study, we tested the hypothesis that H2 alleviates oxidative stress by suppressing xanthine oxidoreductase (XOR) and/or preventing tumor necrosis factor-alfa (TNF-α)-mediated syndecan-1 shedding during EG damage. Methods: HS/R was induced in rats by reducing mean arterial pressure (MAP) to 35 mm Hg for 60 min followed by resuscitation. Rats inhaled oxygen or H2 + oxygen after achieving shock either in the presence or absence of an XOR inhibitor (XOR-I) for both the groups. In a second test, rats received oxygen alone or antitumor necrosis factor (TNF)-α monoclonal antibody with oxygen or H2. Two hours after resuscitation, XOR activity, purine metabolites, cytokines, syndecan-1 were measured and survival rates were assessed 6 h after resuscitation. Results: H2 and XOR-I both suppressed MAP reduction and improved survival rates. H2 did not affect XOR activity and the therapeutic effects of XOR-I and H2 were additive. H2 suppressed plasma TNF-α and syndecan-1 expression; however, no additional H2 therapeutic effect was observed in the presence of anti-TNF-α monoclonal antibody. Conclusions: H2 inhalation after shock stabilized hemodynamics and improved survival rates in an HS/R model independent of XOR. The therapeutic action of H2 was partially mediated by inhibition of TNF-α-dependent syndecan-1 shedding.