Hydrogenology
Hydrogenology editorial study record

Hydrogen gas ameliorates oxidative stress in early brain injury after subarachnoid hemorrhage in rats

Zhan Y, Chen C, Suzuki H, Hu Q, Zhi X, Zhang JH. · Critical Care Medicine. 2012;40(4):1291-1296.

PreclinicalInhaled H₂Published 2012
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

Randomized three-group controlled rat subarachnoid-hemorrhage experiment

Research topic

Other neurological conditions

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

One hundred thirty-seven adult male Sprague-Dawley rats in an endovascular-perforation subarachnoid-hemorrhage model.

Sample

137 rats randomized to sham n=27, SAH n=59 or SAH plus H₂ n=51. Moderate-SAH animals were retained for most outcome analyses; mild and severe cases were excluded according to prespecified severity categories.

Duration

One two-hour exposure starting one hour after hemorrhage; outcomes at 24 and 72 hours.

Intervention

A two-hour chamber exposure began one hour after SAH using premixed 2.9% H₂, 20% O₂ and balance nitrogen.

Hydrogen form

Premixed H₂/O₂/N₂ inhalation — not Brown's gas: the H₂:O₂ proportions were 2.9:20 rather than 2:1.

H₂ specification

Total gas flow was 8 L/min for the first five minutes, then 6 L/min. Therefore H₂ flow was 232 mL/min initially and 174 mL/min during maintenance; O₂ flow was 1,600 mL/min initially and 1,200 mL/min during maintenance. These are direct calculations from the source's reported composition and total flows.

H₂ flow

232 mL/min for the first 5 minutes; 174 mL/min thereafter.

O₂ delivered with H₂

20% O₂: 1,600 mL/min for the first 5 minutes; 1,200 mL/min thereafter.

Comparator

Sham-operated rats and SAH rats breathing the control condition without the H₂ mixture.

Reported, not endorsed

Outcomes and reported result

Outcomes measured

Mortality, hemorrhage grade, neurological score, body weight, brain edema, blood-brain-barrier permeability, apoptosis and lipid/protein/DNA oxidative-damage markers.

Reported result

At 24 hours H₂ reduced edema, barrier leakage, apoptosis and oxidative markers and improved neurological score. Mortality was not significantly different (15.3% vs 9.8%); body weight was unchanged; neurological improvement and edema reduction were absent at 72 hours; Evans-blue reduction at 24 hours was absent in cerebellum and brainstem. The authors described the benefit as transient.

Results-extraction completeness

The complete free PMC article was checked for allocation, exclusions, exact gas composition, total flows, calculated H₂/O₂ flows, timing, 24- and 72-hour positive/null outcomes, limitations, funding and conflicts.

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

Single short exposure in a rat model, severity-based exclusions, many surrogate endpoints, no durable benefit at 72 hours and no human participants. NIH grant support was reported; authors disclosed no potential conflicts.

Applies directly to

Experimental subarachnoid hemorrhage in adult male rats; it does not establish an inhalation treatment for patients.

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: 22336722 · DOI: 10.1097/CCM.0b013e31823da96d

Publisher access

Free full author manuscript in PubMed Central.

Extraction basis

Complete PMC author manuscript and PubMed metadata; full-text extraction checked 9 August 2026.

Record revision

2026-08-10