Hydrogen Gas Fails to Protect Baby Rat Brains from Severe Oxygen Loss
- Authors
- Gerald A. Matchett, Nancy Fathali, Yu Hasegawa, Vikram Jadhav, Robert P. Ostrowski, Robert D. Martin, Ihab R. Dorotta, Xuejun Sun, John H. Zhang
- Journal
- Brain Research
- Year
- 2009
- DOI
- 10.1016/j.brainres.2008.12.066
- Study Type
- Rat
- Outcome
- Neutral
- Peer Reviewed
- Yes
- Country
- United States
- Health Condition
- Neonatal Hypoxia-Ischemia
- Body System
- Nervous System
TL;DR
Breathing hydrogen gas did not help reduce brain damage in newborn rats that experienced moderate to severe lack of oxygen, and it actually increased damage when given before the oxygen loss occurred.
Key Finding
Hydrogen gas therapy at 2.9% concentration failed to reduce brain infarction (tissue death) or oxidative stress markers in moderate and severe neonatal hypoxia-ischemia in rats, and pretreatment with hydrogen gas was associated with increased brain injury.
Summary
Researchers tested whether hydrogen gas could protect newborn rat brains from injury caused by lack of oxygen and blood flow (hypoxia-ischemia). While hydrogen gas had shown promise in mild cases and adult stroke models, this study found that hydrogen gas at 2.9% concentration did not reduce brain damage or markers of cellular damage in moderate and severe cases of newborn brain injury. Surprisingly, giving hydrogen gas before the injury actually increased brain damage.
Practical Takeaway
This rat study suggests that hydrogen gas may not be effective for severe neonatal brain injuries caused by oxygen deprivation, despite its theoretical antioxidant properties. However, this is a laboratory animal study in newborn rats, so results may not directly apply to humans. The findings raise questions about hydrogen gas's clinical use in severe neonatal brain injury cases and suggest more research is needed before clinical application.
Abstract
Hydrogen gas (H(2)) has been shown to ameliorate brain injury in experimental adult rat focal ischemia and in a mild neonatal hypoxia-ischemia (HI, 90 min hypoxia) rat model. In this study we tested H(2) in moderate (120 min hypoxia) and severe (150 min hypoxia) neonatal HI rat models. We hypothesized that H(2) would improve outcomes after neonatal HI by scavenging free radicals. Two hundred (200) unsexed Sprague-Dawley rats at day 10 of life (p10) underwent neonatal HI with the Rice-Vannucci model. Multiple treatment protocols were studied, including pre-ischemic treatment, intra-ischemic treatment, and post-ischemic treatment (Sham n=32, HI n=82, HI+H(2)n=86). We also tested H(2) in middle cerebral artery occlusion (MCAO) in adult rats (MCAO n=9, MCAO+H(2)n=7) for comparison. Analysis at 24 h included infarction volume, measurement of brain concentration of malondialdehyde (MDA) (an end-product of lipid peroxidation), daily weight, Nissl histology, and mortality. In moderate and severe neonatal HI models, hydrogen gas therapy (2.9% concentration H(2)) was not associated with decreased volume of infarction or decreased concentration of MDA. H(2) gas pretreatment (2.9%) was associated with increased infarction volume in neonatal HI. In MCAO in adult rats, H(2) gas therapy demonstrated a trend of beneficial effect. Exposure of H(2) gas to non-ischemic neonates resulted in a significant increase in brain concentration of MDA. We conclude that 2.9% H(2) gas therapy does not ameliorate moderate to severe ischemic damage in neonatal hypoxia-ischemia.