Hydrogen Gas Protects Newborn Brains from Birth Injury in Animal Study

Authors
Journal
Journal of Physiology and Pharmacology
Year
Study Type
Pig
Outcome
Positive
Peer Reviewed
Yes
Country
Hungary
Health Condition
Hypoxic-Ischemic Encephalopathy
Body System
Nervous System

TL;DR

A study on newborn piglets shows that inhaling hydrogen gas can help protect their brains from damage caused by a lack of oxygen and excess carbon dioxide during birth.

Key Finding

Hydrogen gas treatment after oxygen deprivation preserved brain cell function and reduced neuronal injury across multiple brain regions in piglets, with effects likely mediated by reduced oxidative stress.

Summary

Researchers created a pig model that mimics severe oxygen deprivation in newborns (a condition called hypoxic-ischemic encephalopathy) and tested whether hydrogen gas could protect the brain. After inducing asphyxia in anesthetized piglets, they treated some animals with hydrogen gas mixed with air for 4 hours. Hydrogen-treated piglets showed better recovery of brain electrical activity and less neuronal (brain cell) damage across multiple brain regions compared to controls, with signs that hydrogen reduced oxidative stress (cellular damage from unstable molecules).

Practical Takeaway

This animal study suggests hydrogen gas may have neuroprotective potential in severe oxygen deprivation scenarios, but it is a pig study only and does not yet demonstrate safety or effectiveness in human newborns. Much more research, including human clinical trials, would be needed before any therapeutic application in infants could be considered.

Abstract

Hypoxic-ischemic encephalopathy (HIE) is the major consequence of perinatal asphyxia (PA) in term neonates. Although the newborn piglet is an accepted large animal PA/HIE model, there is no consensus on PA-induction methodology to produce clinically relevant HIE. We aimed to create and to characterize a novel PA model faithfully reproducing all features of asphyxiation including severe hypercapnia resulting in HIE, and to test whether H2 is neuroprotective in this model. Piglets were anaesthetised, artificially ventilated, and intensively monitored (electroencephalography, core temperature, O2 saturation, arterial blood pressure and blood gases). Asphyxia (20 min) was induced by ventilation with a hypoxic-hypercapnic (6%O2 - 20%CO2) gas mixture. Asphyxia-induced changes in the cortical microcirculation were assessed with laser-speckle contrast imaging and analysis. Asphyxia was followed by reventilation with air or air containing hydrogen (2.1%H2, 4 hours). After 24 hours survival, the brains were harvested for neuropathology. Our PA model was characterized by the development of severe hypoxia (pO2 = 27 ± 4 mmHg), and combined acidosis (pH = 6.76 ± 0.04; pCO2 = 114 ± 11 mmHg; lactate = 12.12 ± 0.83 mmol/L), however, cortical ischemia did not develop during the stress. Severely depressed electroencephalography (EEG), and marked neuronal injury indicated the development of HIE. H2 was neuroprotective shown both by the enhanced recovery of EEG and by the significant preservation of neurons in the cerebral cortex, hippocampus, basal ganglia, and the thalamus. H2 appeared to reduce oxidative stress shown by attenuation of 8-hydroxy-2'-deoxyguanosine immunostaining. In summary, this new PA piglet model is able to induce moderate/severe HIE, and the efficacy of hydrogen post-treatment to preserve neuronal activity/function in this PA/HIE model suggests the feasibility of this safe and inexpensive approach in the treatment of asphyxiated babies.