Hydrogenology
Hydrogenology editorial study record

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.

PreclinicalInhaled H₂Published 2019
Study record, not medical adviceThis page reports one source and Hydrogenology’s source-text extraction. It does not establish that molecular hydrogen is effective, safe or appropriate for any person. Human, animal and laboratory evidence must not be treated as equivalent.
Source and classification

What kind of evidence is this?

Evidence stream

Preclinical

Reported design

Controlled rat hemorrhagic-shock and resuscitation experiment

Research topic

Critical care and ischemia-reperfusion

Administration classification

Inhaled H₂

Study result signal

Not reported in this record.

Outcome type

Not reported in this record.

Reported in the source

Methods at a glance

Population or model

Rats weighing 300–500 g assigned to sham, hemorrhagic shock/resuscitation or H₂ plus hemorrhagic shock/resuscitation groups.

Sample

Three experimental groups; the article does not state one consolidated animal total in the reported methods, so no total is inferred.

Duration

One hour after shock induction plus three hours after resuscitation.

Intervention

Chamber inhalation during one hour of hemorrhagic shock and three hours after resuscitation.

Hydrogen form

Dilute H₂ in oxygen/nitrogen carrier gas — H₂ alone as the experimental component, not Brown's gas.

H₂ specification

2% H₂, 21% O₂ and 77% N₂ at 4 L/min total chamber flow; control gas was 21% O₂ and 79% N₂.

H₂ flow

80 mL/min H₂, calculated from 2% of the reported 4,000 mL/min chamber flow.

O₂ delivered with H₂

840 mL/min O₂, calculated from 21% of total chamber flow; the same O₂ fraction was used in control gas.

Comparator

Sham and hemorrhagic-shock/resuscitation groups inhaled matched 21% O₂/79% N₂ control gas.

Reported, not endorsed

Outcomes and reported result

Outcomes measured

Arterial PO₂/PCO₂ and lactate, lung histology, inflammatory-cell infiltration, myeloperoxidase activity and pulmonary inflammatory mediators.

Reported result

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.

Results-extraction completeness

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. Null findings, outcome type, study design and precision all matter.

Interpretation limits

Cautions and applicability

Design and reporting cautions

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.

Applies directly to

Rat hemorrhagic-shock/resuscitation lung-injury model only.

Preliminary appraisal framework

Not reported in this record.

Preliminary risk-of-bias status

Not reported in this record.

Appraisal rationale

Not reported in this record.

No single-study GRADE certainty rating is assigned. Certainty is assessed by important outcome across a complete eligible evidence set, not by attaching a final grade to one source.

Provenance

Sources and record status

Identifiers

PMID: 31179095 · DOI: 10.21037/jtd.2019.03.23

Publisher access

Free full article on the journal site and PubMed Central.

Extraction basis

Journal of Thoracic Disease and PMC full articles plus PubMed metadata; full-text and article-status check completed 8 August 2026.

Record revision

2026-08-10