Hydrogen Gas and Solution Don't Protect Against Spinal Cord Injury
- Authors
- Atsuo Yamashita, Takehiko Fukui, Satoshi Yamashita, Kazuyoshi Ishida, Mishiya Matsumoto
- Journal
- Journal of Anesthesia
- Year
- 2024
- DOI
- 10.1007/s00540-024-03334-4
- Study Type
- Rabbit
- Outcome
- Neutral
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Spinal Cord Injury
- Body System
- Nervous System
TL;DR
Inhaling hydrogen gas and injecting a hydrogen-rich solution did not prevent spinal cord damage from lack of blood flow in rabbits.
Key Finding
Neither hydrogen gas inhalation nor hydrogen-rich solution administration—alone or combined—protected rabbit spinal cords from ischemic injury, and the solution delivered minimal hydrogen to spinal cord tissue.
Summary
Researchers tested whether hydrogen gas (breathed in) and hydrogen-rich salt solution (injected) could protect rabbit spinal cords from damage caused by temporarily cutting off blood flow. Neither treatment alone nor the combination of both treatments reduced spinal cord injury compared to untreated rabbits. The hydrogen-rich solution delivered very little hydrogen to the spinal cord tissue compared to breathing hydrogen gas.
Practical Takeaway
This animal study suggests that hydrogen-rich solutions may not deliver enough hydrogen to spinal cord tissue to be effective, at least using the methods tested. However, this is a single rabbit study with a small sample size, so results may not apply to humans or to different hydrogen delivery approaches. More research would be needed before drawing conclusions about hydrogen water's potential for spinal cord injury.
Abstract
Purpose: This study aimed to determine whether the combination of H2 gas inhalation and administration of hydrogen-rich acetated Ringer's solution (HS) could protect against ischemic spinal cord injury in rabbits. Methods: In Experiment 1, rabbits were randomly assigned to a 1.2% H2 gas group, HS group, 1.2% H2 gas + HS group (combination group), or control group (n = 6 per group). The H2 concentration of HS was 0.65 mM. H2 was inhaled for 60 min, starting 5 min before reperfusion. HS (20 mL/kg) was divided into six bolus injections at 10-min intervals, starting 5 min before reperfusion. Spinal cord ischemia was produced by occluding the abdominal aorta for 15 min. Neurologic and histopathologic evaluations were performed 7 days after reperfusion. In Experiment 2, H2 concentrations in spinal cord tissue according to the administration of 1.2% H2 gas or HS were compared by measuring the electric current through a platinum needle electrode (n = 2). In Experiment 3, rabbits were assigned to a 2% H2 gas group or control group (n = 6 per group). Spinal cord ischemia was produced and neurologic and histopathologic evaluations were performed as in Experiment 1. Results: There were no significant differences among the groups in the neurologic and histopathologic outcomes in Experiments 1 and 3. Bolus administration of HS (10 mL) transiently increased the current to only 1/30th and 1/27th of the plateau current with 1.2% H2 gas inhalation in two animals. Conclusion: These results suggest that the combination of 1.2% H2 gas inhalation and administration of a hydrogen-rich solution does not protect against ischemic spinal cord injury and that the increase in H2 concentration in spinal cord tissue after administration of HS is very low compared to 1.2% H2 gas inhalation. Keywords: Hydrogen gas; Hydrogen-rich solution; Rabbit; Spinal cord ischemia.