Hydrogen Gas Protects Newborn Brain from Birth Asphyxia Damage

Authors
Journal
Pediatric Research
Year
DOI
10.1203/PDR.0b013e3181f2e81c
Study Type
Pig
Outcome
Positive
Peer Reviewed
Yes
Country
Hungary
Health Condition
Birth Asphyxia
Body System
Nervous System

TL;DR

Breathing air supplemented with a small amount of hydrogen gas can reduce brain damage and improve blood vessel function in the brains of newborn pigs after a lack of oxygen.

Key Finding

Hydrogen-supplemented ventilation significantly reduced brain cell injury across multiple brain regions and preserved blood vessel function in newborn pigs after oxygen deprivation.

Summary

Researchers tested whether hydrogen gas added to breathing air could protect newborn pig brains from damage caused by oxygen deprivation (asphyxia). After 10 minutes without oxygen followed by 4 hours of breathing hydrogen-supplemented air, piglets that received hydrogen showed less brain cell damage across multiple brain regions and better blood vessel function compared to those breathing regular air. The protective effect appears to work by neutralizing harmful molecules called reactive oxygen species that form during oxygen deprivation.

Practical Takeaway

This animal study suggests hydrogen gas may have neuroprotective potential for newborns experiencing asphyxia, but it is a pig study only and does not yet demonstrate safety or effectiveness in humans. Much more research, including human clinical trials, would be needed before this approach could be considered for medical use in newborns.

Abstract

Hydrogen (H2) has been reported to neutralize toxic reactive oxygen species. Oxidative stress is an important mechanism of neuronal damage after perinatal asphyxia. We examined whether 2.1% H2-supplemented room air (H2-RA) ventilation would preserve cerebrovascular reactivity (CR) and brain morphology after asphyxia/reventilation (A/R) in newborn pigs. Anesthetized, ventilated piglets were assigned to one of the following groups: A/R with RA or H2-RA ventilation (A/R-RA and A/R-H2-RA; n = 8 and 7, respectively) and respective time control groups (n = 9 and 7). Asphyxia was induced by suspending ventilation for 10 min, followed by reventilation with the respective gases for 4 h. After euthanasia, the brains were processed for neuropathological examination. Pial arteriolar diameter changes to graded hypercapnia (5-10% CO2 inhalation), and NMDA (10(-4) M) were determined using the closed cranial window/intravital microscopy before and 1 h after asphyxia. Neuropathology revealed that H2-RA ventilation significantly reduced neuronal injury induced by A/R in virtually all examined brain regions including the cerebral cortex, the hippocampus, basal ganglia, cerebellum, and the brainstem. Furthermore, H2-RA ventilation significantly increased CR to hypercapnia after A/R (% vasodilation was 23 ± 4% versus 41 ± 9%, p < 0.05). H2-RA ventilation did not affect reactive oxygen species-dependent CR to NMDA. In summary, H2-RA could be a promising approach to reduce the neurologic deficits after perinatal asphyxia.