Hydrogen Gas Doesn't Help Brain-Cooling Therapy for Birth Injuries
- Authors
- Viktória Kovács, Gábor Remzső, Valéria Tóth-Szűki, Viktória Varga, János Németh, Ferenc Domoki
- Journal
- International Journal of Molecular Sciences
- Year
- 2020
- DOI
- 10.3390/ijms21186801
- Study Type
- Pig
- Outcome
- Neutral
- Peer Reviewed
- Yes
- Country
- Hungary
- Health Condition
- Hypoxic-Ischemic Encephalopathy
- Body System
- Nervous System
TL;DR
Adding molecular hydrogen or carbon dioxide to therapeutic hypothermia treatment does not improve brain protection in newborn piglets with brain injury due to oxygen deprivation.
Key Finding
Inhaled hydrogen gas and carbon dioxide did not improve the brain-protective effects of therapeutic hypothermia in a neonatal brain injury model, and carbon dioxide actually reduced hypothermia's protective effect in one brain region.
Summary
Researchers tested whether adding hydrogen gas or carbon dioxide to standard cooling therapy would improve brain protection in newborn piglets with hypoxic-ischemic encephalopathy (a brain injury caused by lack of oxygen and blood flow). While cooling therapy alone protected one brain region (the caudate nucleus), adding either gas did not help—and carbon dioxide actually made the cooling therapy less effective. The study suggests these gases are not useful additions to current treatment.
Practical Takeaway
This animal study suggests that hydrogen gas inhalation may not enhance the standard cooling treatment for severe newborn brain injury. However, this is a single piglet study with specific conditions, so results cannot be directly applied to humans. More research would be needed before drawing conclusions about hydrogen's usefulness in this medical context.
Abstract
Hypoxic-ischemic encephalopathy (HIE) is still a major cause of neonatal death and disability as therapeutic hypothermia (TH) alone cannot afford sufficient neuroprotection. The present study investigated whether ventilation with molecular hydrogen (2.1% H2) or graded restoration of normocapnia with CO2 for 4 h after asphyxia would augment the neuroprotective effect of TH in a subacute (48 h) HIE piglet model. Piglets were randomized to untreated naïve, control-normothermia, asphyxia-normothermia (20-min 4%O2-20%CO2 ventilation; Tcore = 38.5 °C), asphyxia-hypothermia (A-HT, Tcore = 33.5 °C, 2-36 h post-asphyxia), A-HT + H2, or A-HT + CO2 treatment groups. Asphyxia elicited severe hypoxia (pO2 = 19 ± 5 mmHg) and mixed acidosis (pH = 6.79 ± 0.10). HIE development was confirmed by altered cerebral electrical activity and neuropathology. TH was significantly neuroprotective in the caudate nucleus but demonstrated virtually no such effect in the hippocampus. The mRNA levels of apoptosis-inducing factor and caspase-3 showed a ~10-fold increase in the A-HT group compared to naïve animals in the hippocampus but not in the caudate nucleus coinciding with the region-specific neuroprotective effect of TH. H2 or CO2 did not augment TH-induced neuroprotection in any brain areas; rather, CO2 even abolished the neuroprotective effect of TH in the caudate nucleus. In conclusion, the present findings do not support the use of these medical gases to supplement TH in HIE management.