Hydrogen Gas Inhalation Attenuates Endothelial Glycocalyx Damage and Stabilizes Hemodynamics in a Rat Hemorrhagic Shock Model.
Tomoyoshi Tamura, Motoaki Sano, Tadashi Matsuoka, Joe Yoshizawa, Ryo Yamamoto, Yoshinori Katsumata, Jin Endo, Koichiro Homma, Mayumi Kajimura, Masaru Suzuki, Eiji Kobayashi, Junichi Sasaki · Shock (Augusta, Ga.) · 2020
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Independent study record
Each H2HUBB study page organizes source-linked research details for educational use. Interpretation should remain proportional to the study design, population, controls, and limitations.
H2HUBB TAKEAWAY
In rats, H₂ and XOR-I both suppressed MAP reduction and improved survival rates. These results are preclinical and suggest molecular hydrogen's therapeutic potential in the condition studied. Further human research is needed to establish clinical effectiveness.
What the Researchers Studied
In this study, the researchers 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.
How Molecular Hydrogen Was Used
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.
What the Researchers Found
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.
H₂ Mechanisms / Biological Findings
The source material reviewed did not establish a specific molecular hydrogen mechanism for the reported findings.
Authors’ Conclusion
The authors concluded that 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.