Hydrogen gas inhalation ameliorates lung injury after hemorrhagic shock and resuscitation
Moon DH, Kang DY, Haam SJ, Yumoto T, Tsukahara K, Yamada T, Nakao A, Lee S. · Journal of Thoracic Disease. 2019;11(4):1519–1527.
Study at a glance
Preclinical
Rats weighing 300–500 g assigned to sham, hemorrhagic shock/resuscitation or H₂ plus hemorrhagic shock/resuscitation groups.
Chamber inhalation during one hour of hemorrhagic shock and three hours after resuscitation. · 2% H₂, 21% O₂ and 77% N₂ at 4 L/min total chamber flow; control gas was 21% O₂ and 79% N₂.
One hour after shock induction plus three hours after resuscitation.
PO₂ differences between shock groups were not statistically significant and PCO₂ was null across groups. Lactate, inflammatory infiltration, MPO and most inflammatory mediators were lower with H₂ than shock control; several H₂ values remained above sham. The study measured short-term surrogate and tissue outcomes, not survival or clinical recovery.
Preclinical, short-term three-group experiment with no reported consolidated animal total and multiple molecular outcomes. It does not establish benefit in people. Korean National Research Foundation funding was reported and authors declared no conflicts.
What kind of evidence is this?
Preclinical
Controlled rat hemorrhagic-shock and resuscitation experiment
Critical care and ischemia-reperfusion
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
Rats weighing 300–500 g assigned to sham, hemorrhagic shock/resuscitation or H₂ plus hemorrhagic shock/resuscitation groups.
Three experimental groups; the article does not state one consolidated animal total in the reported methods, so no total is inferred.
One hour after shock induction plus three hours after resuscitation.
Chamber inhalation during one hour of hemorrhagic shock and three hours after resuscitation.
Dilute H₂ in oxygen/nitrogen carrier gas — H₂ alone as the experimental component, not Brown's gas.
2% H₂, 21% O₂ and 77% N₂ at 4 L/min total chamber flow; control gas was 21% O₂ and 79% N₂.
80 mL/min H₂, calculated from 2% of the reported 4,000 mL/min chamber flow.
840 mL/min O₂, calculated from 21% of total chamber flow; the same O₂ fraction was used in control gas.
Sham and hemorrhagic-shock/resuscitation groups inhaled matched 21% O₂/79% N₂ control gas.
Outcomes and reported result
Arterial PO₂/PCO₂ and lactate, lung histology, inflammatory-cell infiltration, myeloperoxidase activity and pulmonary inflammatory mediators.
PO₂ differences between shock groups were not statistically significant and PCO₂ was null across groups. Lactate, inflammatory infiltration, MPO and most inflammatory mediators were lower with H₂ than shock control; several H₂ values remained above sham. The study measured short-term surrogate and tissue outcomes, not survival or clinical recovery.
The complete Journal of Thoracic Disease/PMC article, gas composition and chamber flow, blood-gas null findings, histology, inflammatory tables, funding and conflicts were checked.
A reported association, difference or mechanism is not automatically a clinical benefit.
Limitations and applicability
Preclinical, short-term three-group experiment with no reported consolidated animal total and multiple molecular outcomes. It does not establish benefit in people. Korean National Research Foundation funding was reported and authors declared no conflicts.
Rat hemorrhagic-shock/resuscitation lung-injury model only.
No single-study GRADE certainty rating is assigned. Read how records and evidence assessments are prepared.
Sources and record status
PMID: 31179095 · DOI: 10.21037/jtd.2019.03.23
Free full article on the journal site and PubMed Central.
Journal of Thoracic Disease and PMC full articles plus PubMed metadata; full-text and article-status check completed 8 August 2026.
10 August 2026
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