Hydrogen Gas Protects Spinal Cord from Injury in Animal Study
- Authors
- Aya Kimura, Koichi Suehiro, Akira Mukai, Yohei Fujimoto, Tomoharu Funao, Tokuhiro Yamada, Takashi Mori
- Journal
- The Journal of Thoracic and Cardiovascular Surgery
- Year
- 2021
- DOI
- 10.1016/j.jtcvs.2021.04.077
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Spinal Cord Ischemia-Reperfusion Injury
- Body System
- Nervous System
TL;DR
Breathing in hydrogen gas can help protect the spinal cord from damage caused by temporary loss of blood flow, and it works better at higher concentrations.
Key Finding
Inhaling 3% hydrogen gas significantly reduced harmful glutamate buildup in the spinal cord after ischemia-reperfusion injury in rats, with protection increasing at higher hydrogen concentrations.
Summary
Researchers exposed rats to a spinal cord injury caused by temporarily cutting off blood flow, then restoring it. They tested whether breathing hydrogen gas could reduce damage by measuring glutamate (a chemical that can harm nerve cells when it builds up too much). Breathing 3% hydrogen gas reduced the harmful glutamate buildup and protected nerve cells by activating a cleanup protein called glutamate transporter-1, with higher concentrations of hydrogen gas showing stronger protective effects.
Practical Takeaway
This rat study suggests hydrogen gas inhalation may protect nerve tissue during spinal cord injury by reducing toxic glutamate accumulation. However, this is early-stage animal research; human studies are needed to determine if these findings apply to people and what hydrogen gas delivery methods would be safe and effective.
Abstract
Objective: This experimental study aimed to assess the efficacy of hydrogen gas inhalation against spinal cord ischemia–reperfusion injury and reveal its mechanism by measuring glutamate concentration in the ventral horn using an in vivo microdialysis method. Methods: Male Sprague-Dawley rats were divided into the following 6 groups: sham, only spinal ischemia, 3% hydrogen gas (spinal ischemia + 3% hydrogen gas), 2% hydrogen gas (spinal ischemia + 2% hydrogen gas), 1% hydrogen gas (spinal ischemia + 1% hydrogen gas), and hydrogen gas dihydrokainate (spinal ischemia + dihydrokainate [selective inhibitor of glutamate transporter-1] + 3% hydrogen gas). Hydrogen gas inhalation was initiated 10 minutes before the ischemia. For the hydrogen gas dihydrokainate group, glutamate transporter-1 inhibitor was administered 20 minutes before the ischemia. Immunofluorescence was performed to assess the expression of glutamate transporter-1 in the ventral horn. Results: The increase in extracellular glutamate induced by spinal ischemia was significantly suppressed by 3% hydrogen gas inhalation (P < .05). This effect was produced in increasing order: 1%, 2%, and 3%. Conversely, the preadministration of glutamate transporter-1 inhibitor diminished the suppression of spinal ischemia-induced glutamate increase observed during the inhalation of 3% hydrogen gas. Immunofluorescence indicated the expression of glutamate transporter-1 in the spinal ischemia group was significantly decreased compared with the sham group, which was attenuated by 3% hydrogen gas inhalation (P < .05). Conclusions: Our study demonstrated hydrogen gas inhalation exhibits a protective and concentration-dependent effect against spinal ischemic injury, and glutamate transporter-1 has an important role in the protective effects against spinal cord injury.