Hydrogen Gas Protects Newborn Brain Blood Vessels After Birth Asphyxia

Authors
Journal
Neonatology
Year
DOI
10.1159/000348445
Study Type
Pig
Outcome
Positive
Peer Reviewed
Yes
Country
Hungary
Health Condition
Birth Asphyxia
Body System
Nervous System

TL;DR

Inhaling hydrogen gas can help protect the brain's blood vessels and improve brain function in newborn pigs after a mild lack of oxygen and blood flow.

Key Finding

Hydrogen gas treatment preserved the brain's blood vessel function 24 hours after oxygen deprivation in newborn pigs, whereas untreated animals showed significant impairment in how their blood vessels responded to key stimuli.

Summary

This study examined whether hydrogen gas could protect the brain's blood vessels and nerve cells after a severe lack of oxygen in newborn pigs. Researchers induced asphyxia (oxygen deprivation) in piglets and then treated some with hydrogen gas while others received regular air. Twenty-four hours later, they tested how well the brain's blood vessels responded to different stimuli. The piglets treated with hydrogen showed better preservation of normal blood vessel responses and modest protection against brain cell damage compared to untreated animals.

Practical Takeaway

This animal study suggests hydrogen gas may help protect the developing brain after birth asphyxia by maintaining proper blood vessel function. However, this research was conducted only in pigs, and human studies would be needed to determine if these findings apply to newborn infants. The modest neuroprotective effects observed warrant further investigation before any clinical applications could be considered.

Abstract

<b><i>Background:</i></b> The neurovascular unit encompasses the functional interactions of cerebrovascular and brain parenchymal cells necessary for the metabolic homeostasis of neurons. Previous studies indicated marked but only transient (1-4 h) reactive oxygen species-dependent neurovascular dysfunction in newborn pigs after severe hypoxic/ischemic (H/I) stress contributing to the neuronal injury after birth asphyxia. <b><i>Objectives:</i></b> Our major purpose was to determine if neurovascular dysfunction would also occur later, at 24 h after a milder H/I stress. We also tested if the putative hydroxyl radical scavenger hydrogen (H<sub>2</sub>) exerted neurovascular protection. <b><i>Methods:</i></b> Anesthetized, ventilated piglets were assigned to three groups of 9 animals: time control, asphyxia/reventilation with air, and asphyxia/reventilation with air +2.1% H<sub>2</sub> for 4 h. Asphyxia was induced by suspending ventilation for 8 min. Cerebrovascular reactivity (CR) of pial arterioles was determined using closed cranial window/intravital microscopy 24 h after asphyxia to the endothelium-dependent cerebrovascular stimulus hypercapnia, the neuronal function-dependent stimulus N-methyl-<smlcap>D</smlcap>-aspartate (NMDA), norepinephrine, and sodium nitroprusside. The brains were subjected to histopathology. <b><i>Results:</i></b> Hemodynamic parameters, blood gases, and core temperature did not differ significantly among the experimental groups. In the early reventilation period, the recovery of electroencephalographic activity was significantly better in H<sub>2</sub>-treated animals. Asphyxia/reventilation severely attenuated CR to hypercapnia and NMDA; however, reactivity to norepinephrine and sodium nitroprusside were unaltered. H<sub>2</sub> fully or partially preserved CR to hypercapnia or NMDA, respectively. Histopathology revealed modest neuroprotection afforded by H<sub>2</sub>. <b><i>Conclusions:</i></b> Severe stimulus-selective delayed neurovascular dysfunction develops and persists even after mild H/I stress. H<sub>2</sub> alleviates this delayed neurovascular dysfunction that can contribute to its neuroprotective effect.