Evidence map›Paper›PMID 32804466›Full record

ArticleShock (Augusta, Ga.)2020

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 and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Shock (Augusta, Ga.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 29 citations in OpenAlex.

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  4. Resuscitating the Endothelial Glycocalyx in Trauma and Hemorrhagic Shock.Annals of surgery open : perspectives of surgical history, education, and clinical approaches · 2023
    Review
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  14. Low-Flow Nasal Cannula Hydrogen Therapy.Journal of clinical medicine research · 2020
    Article
  15. What's New in Shock, September 2020?Shock (Augusta, Ga.) · 2020
    Article
  16. Article
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

Tomoyoshi TamuraDepartment of Emergency and Critical Care Medicine, Keio University School of Medicine, Tokyo, Japan.
Motoaki SanoThe Center for Molecular Hydrogen Medicine, Keio University, Tokyo, Japan.
Tadashi MatsuokaDepartment of Emergency and Critical Care Medicine, Keio University School of Medicine, Tokyo, Japan.
Joe YoshizawaDepartment of Emergency and Critical Care Medicine, Keio University School of Medicine, Tokyo, Japan.
Ryo YamamotoDepartment of Emergency and Critical Care Medicine, Keio University School of Medicine, Tokyo, Japan.
Yoshinori KatsumataThe Center for Molecular Hydrogen Medicine, Keio University, Tokyo, Japan.
Jin EndoThe Center for Molecular Hydrogen Medicine, Keio University, Tokyo, Japan.
Koichiro HommaDepartment of Emergency and Critical Care Medicine, Keio University School of Medicine, Tokyo, Japan.
Mayumi KajimuraThe Center for Molecular Hydrogen Medicine, Keio University, Tokyo, Japan.
Masaru SuzukiThe Center for Molecular Hydrogen Medicine, Keio University, Tokyo, Japan.
Eiji KobayashiThe Center for Molecular Hydrogen Medicine, Keio University, Tokyo, Japan.
Junichi SasakiDepartment of Emergency and Critical Care Medicine, Keio University School of Medicine, Tokyo, Japan.
Keio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHydrogen 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.

methodsHS/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.

resultsH2 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.

conclusionsH2 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.

Indexed as

AnimalsArterial PressureDisease Models, AnimalGlycocalyxHemodynamicsHydrogenRatsShock, HemorrhagicSyndecan-1HydrogenSyndecan-1

Identifiers

PMID32804466
PMCPMC7458091
OpenAlexW2982060984

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.