Hydrogen Gas Helps Protect Brain After Stroke in Rat Study
- Authors
- Toru Yoshiura, Satoko Kawauchi, Sho Nishida, Sho Sato, Daichi Hagita, Arumu Endo, Masaya Nakagawa, Takashi Fujii, Yohei Otsuka, Yumiko Mishima, Fujii Kazuya, Satoru Takeuchi, Arata Tomiyama, Terushige Toyooka, Shunichi Sato, Shunichi, Kojiro Wada
- Journal
- Neurotherapeutics
- Year
- 2025
- DOI
- 10.1016/j.neurot.2025.e00617
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Subarachnoid Hemorrhage
- Body System
- Nervous System
TL;DR
Inhaling hydrogen gas and receiving magnesium injections in the spine may help reduce brain damage after a type of stroke in rats.
Key Finding
In rats with simulated subarachnoid hemorrhage, inhaled hydrogen gas and magnesium sulfate both significantly reduced the duration of cortical spreading depolarization (abnormal electrical waves in the brain) and the time the brain spent without adequate blood flow.
Summary
This study tested whether inhaled hydrogen gas and magnesium could protect the brain in rats that had experienced a type of stroke called subarachnoid hemorrhage. Researchers measured brain electrical activity and blood flow after inducing the stroke condition. Both hydrogen and magnesium reduced the duration of abnormal electrical waves in the brain and improved blood flow to brain tissue, with hydrogen working particularly quickly.
Practical Takeaway
While this rat study suggests hydrogen inhalation may help protect brain tissue during certain types of stroke, it is a preliminary animal study and does not yet demonstrate safety or effectiveness in humans. The treatments did not improve measurable neurological outcomes in these rats, which limits the strength of the findings. Human clinical trials would be needed before any conclusions could be drawn about potential benefits for stroke patients.
Abstract
This study investigated whether inhaled hydrogen and intrathecal magnesium could mitigate cortical spreading depolarization and delayed cerebral ischemia in a rat model of subarachnoid hemorrhage. Adult male rats underwent subarachnoid hemorrhage induction with nitric oxide synthase inhibition and high-potassium application to elicit cortical spreading depolarization. Animals were assigned to sham, control, H2, Mg, or combined H2 and Mg treatment groups. We measured direct current potentials, cerebral blood flow, brain water content, bodyweight changes, and neurological outcomes. Compared with controls, the H2 and Mg groups had significantly reduced total depolarization and hypoperfusion times. The combined treatment produced similar benefits. H2 alone rapidly shortened depolarization duration, suggesting that it may offer neuroprotection until Mg effects fully manifest. Neither treatment altered physiological parameters, brain water content, bodyweight, or neurological deficits. These findings indicate that H2 and Mg reduce key pathophysiological processes related to early brain injury and delayed cerebral ischemia following subarachnoid hemorrhage, potentially improving outcomes by minimizing depolarization events and associated ischemia. H2 therapy may provide early protective effects before Mg exertion.