Hydrogen gas distribution in organs after inhalation: Real-time monitoring of tissue hydrogen concentration in rat
Yamamoto R, Homma K, Suzuki S, Sano M, Sasaki J. · Scientific Reports. 2019;9:1255.
Study at a glance
Preclinical
Anesthetized eight-week-old male Sprague-Dawley rats.
Continuous gas inhalation through a face/head hood until the selected tissue reached a concentration plateau, followed by monitoring until return to baseline. · 3% H₂ in air at a validated total flow of 0.2 L/min.
H₂ continued until tissue saturation; median timing was organ-specific, with saturation at about 6.3–9.4 minutes in brain, liver, kidney and mesenteric fat and 20.1 minutes in thigh muscle.
Maximum concentration was highest in liver (29.0±2.6 µmol/L) and lowest in kidney (18.0±2.2 µmol/L). Muscle saturated more slowly than all other tested tissues; onset delay was similar across organs. The study measured distribution, not therapeutic benefit.
Distribution study in anesthetized male rats, one concentration/route, no therapeutic outcome, different animals for different organs, no arterial-blood H₂ measurement and occasional small negative sensor values attributed to measurement effects. A Japanese KAKENHI grant supported the work; no commercial conflict statement was identified on the publisher page, so absence of conflicts is not inferred.
What kind of evidence is this?
Preclinical
In-vivo pharmacokinetic/distribution experiment with real-time microsensor monitoring
Other molecular hydrogen research
Inhaled H₂
Information not yet classified
Some editorial classification fields are still pending. The source-reported outcomes and result are shown below; Hydrogenology does not infer a positive or negative signal from prose automatically.
Methods
Anesthetized eight-week-old male Sprague-Dawley rats.
One organ was monitored per animal; assay counts were brain n=8, liver n=6, kidney n=5, mesenteric fat n=4 and thigh muscle n=5. The article does not state a consolidated unique-rat total.
H₂ continued until tissue saturation; median timing was organ-specific, with saturation at about 6.3–9.4 minutes in brain, liver, kidney and mesenteric fat and 20.1 minutes in thigh muscle.
Continuous gas inhalation through a face/head hood until the selected tissue reached a concentration plateau, followed by monitoring until return to baseline.
H₂ alone mixed into air — not Brown's gas.
3% H₂ in air at a validated total flow of 0.2 L/min.
6 mL/min H₂, calculated from 200 mL/min total flow × 3% H₂.
Approximately 21% O₂ in the air carrier; approximately 42 mL/min O₂ calculated from 200 mL/min × 21%.
Within-study comparison across organs and tissues; there was no separate non-H₂ control group for the concentration curves.
Outcomes and reported result
Maximum tissue H₂ concentration, time to 10%, 63%, 90% and full saturation, and washout dynamics in brain, liver, kidney, mesenteric fat and thigh muscle.
Maximum concentration was highest in liver (29.0±2.6 µmol/L) and lowest in kidney (18.0±2.2 µmol/L). Muscle saturated more slowly than all other tested tissues; onset delay was similar across organs. The study measured distribution, not therapeutic benefit.
The complete open-access publisher article, gas concentration and flow, assay counts, all principal distribution results, measurement limitations, funding and author disclosures were checked.
A reported association, difference or mechanism is not automatically a clinical benefit.
Limitations and applicability
Distribution study in anesthetized male rats, one concentration/route, no therapeutic outcome, different animals for different organs, no arterial-blood H₂ measurement and occasional small negative sensor values attributed to measurement effects. A Japanese KAKENHI grant supported the work; no commercial conflict statement was identified on the publisher page, so absence of conflicts is not inferred.
Describes tissue exposure kinetics under this rat protocol; it does not establish an effective or safe clinical dose.
No single-study GRADE certainty rating is assigned. Read how records and evidence assessments are prepared.
Sources and record status
PMID: 30718910 · DOI: 10.1038/s41598-018-38180-4
Open-access Scientific Reports article and PubMed Central copy.
Scientific Reports publisher article, PubMed Central copy and PubMed metadata; full-text extraction checked 9 August 2026.
10 August 2026
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