Combined early fluid resuscitation and hydrogen inhalation attenuates lung and intestine injury
Liu W, Shan LP, Dong XS, Liu XW, Ma T, Liu Z. · World Journal of Gastroenterology. 2013;19(4):492–502.
Study at a glance
Preclinical
Male Wistar rats with lipopolysaccharide-induced septic shock, mechanically ventilated under anesthesia.
The H₂ group received early fluid challenges and vasopressor support according to the reported hemodynamic protocol while breathing 2% H₂ in air through a tracheal ventilator. · 2% H₂ in air; ventilation frequency was 100 breaths/min with tidal volume 10 mL/kg.
H₂ was delivered during the acute ventilated shock/resuscitation experiment; animals were killed two hours after septic shock was established. The article does not state a separate exact H₂ start-to-stop duration.
Compared with fluid resuscitation alone, the combined H₂ group had lower lactate, fluid and norepinephrine requirements and less lung and intestinal oxidative, inflammatory and histological injury. Mean arterial pressure and heart rate did not differ between the two resuscitation groups, and PaCO₂ did not differ among all four groups. Several comparisons between shock alone and fluid resuscitation alone were also non-significant or unfavorable.
Acute preclinical endotoxin model, combined intervention, many surrogate endpoints and no separate H₂-only arm, so the H₂-specific contribution cannot be isolated. Total gas flow and exact inhalation duration are not stated. No dedicated funding or conflict-of-interest declaration was identified in the checked article, so absence is not inferred.
What kind of evidence is this?
Preclinical
Randomized four-group rat endotoxin-shock 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
Male Wistar rats with lipopolysaccharide-induced septic shock, mechanically ventilated under anesthesia.
60 rats randomized equally: healthy control n=15, septic shock n=15, septic shock plus early fluid resuscitation n=15, and septic shock plus early fluid resuscitation and H₂ n=15.
H₂ was delivered during the acute ventilated shock/resuscitation experiment; animals were killed two hours after septic shock was established. The article does not state a separate exact H₂ start-to-stop duration.
The H₂ group received early fluid challenges and vasopressor support according to the reported hemodynamic protocol while breathing 2% H₂ in air through a tracheal ventilator.
H₂ alone diluted in room air — not Brown's gas.
2% H₂ in air; ventilation frequency was 100 breaths/min with tidal volume 10 mL/kg.
Not reported — ventilation settings and H₂ percentage are given, but total minute flow including circuit losses is not reported, so H₂ mL/min cannot be calculated reliably.
Approximately the oxygen fraction of room air; neither a measured O₂ fraction nor O₂ flow in mL/min is reported.
Septic shock plus the same early fluid-resuscitation protocol without H₂, septic shock without early resuscitation and healthy ventilated controls.
Outcomes and reported result
Hemodynamics, arterial blood gases, fluid and norepinephrine requirements, lung wet/dry ratio and histology, intestinal Chiu score, oxidative-stress enzymes and products, cytokines, Fas and Bcl-2.
Compared with fluid resuscitation alone, the combined H₂ group had lower lactate, fluid and norepinephrine requirements and less lung and intestinal oxidative, inflammatory and histological injury. Mean arterial pressure and heart rate did not differ between the two resuscitation groups, and PaCO₂ did not differ among all four groups. Several comparisons between shock alone and fluid resuscitation alone were also non-significant or unfavorable.
The complete open-access article, randomization and group sizes, ventilation and resuscitation protocols, gas composition, positive and null results and article disclosures were checked.
A reported association, difference or mechanism is not automatically a clinical benefit.
Limitations and applicability
Acute preclinical endotoxin model, combined intervention, many surrogate endpoints and no separate H₂-only arm, so the H₂-specific contribution cannot be isolated. Total gas flow and exact inhalation duration are not stated. No dedicated funding or conflict-of-interest declaration was identified in the checked article, so absence is not inferred.
Experimental septic shock in rats receiving invasive ventilation and protocolized resuscitation; not evidence of clinical benefit in people with sepsis.
No single-study GRADE certainty rating is assigned. Read how records and evidence assessments are prepared.
Sources and record status
PMID: 23382627 · DOI: 10.3748/wjg.v19.i4.492
Open-access PubMed Central and publisher article.
Complete PubMed Central/publisher article and PubMed metadata; full-text extraction checked 9 August 2026.
10 August 2026
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