Hydrogen Gas Protects Blood Vessels During Shock in Rats
- Authors
- Tsunehisa Sato, Soichiro Mimuro, Takasumi Katoh, Tadayoshi Kurita, Sang Kien Truong, Kensuke Kobayashi, Hiroshi Makino, Matsuyuki Doi, Yoshiki Nakajima
- Journal
- Journal of Anesthesia
- Year
- 2020
- DOI
- 10.1007/s00540-020-02737-3
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Hemorrhagic Shock
- Body System
- Cardiovascular
TL;DR
Breathing in a low concentration of hydrogen gas helped protect blood vessel linings and increased survival time in rats experiencing severe blood loss.
Key Finding
Rats inhaling 1.2% hydrogen gas during hemorrhagic shock had significantly thicker endothelial glycocalyx and survived about 81 minutes longer than control rats, though this was a laboratory study in animals, not humans.
Summary
In this rat study, researchers investigated whether inhaling hydrogen gas could protect the endothelial glycocalyx (a protective layer lining blood vessels) during severe blood loss. Rats that inhaled 1.2% hydrogen gas and experienced simulated hemorrhagic shock had thicker protective layers on their blood vessels, lower levels of a marker indicating vessel damage, and survived longer than rats that did not receive hydrogen gas. Interestingly, a higher concentration of hydrogen (3.0%) did not produce the same benefits, suggesting that the dose matters.
Practical Takeaway
While this rat study suggests hydrogen gas inhalation may protect blood vessel linings during severe shock, it is an animal-only study and cannot be directly applied to humans. The finding that 1.2% hydrogen worked better than 3.0% suggests concentration matters, but much more research—including human studies—would be needed before any clinical recommendations could be made.
Abstract
Purpose Hydrogen gas (H2) inhalation improved the survival rate of hemorrhagic shock. However, its mechanisms are unknown. We hypothesized that H2 protected the endothelial glycocalyx during hemorrhagic shock and prolonged survival time. Methods 83 Sprague–Dawley rats were anesthetized with isoflurane. The animals were randomly assigned to 5 groups: room air with no shock, 1.2% H2 with no shock, room air with shock (Control-S), 1.2% H2 with shock (H21.2%-S), and 3.0% H2 with shock (H23.0%-S). Shock groups were bled to a mean arterial pressure of 30–35 mmHg and held for 60 min, then resuscitated with normal saline at fourfold the amount of the shed blood volume. Results The syndecan-1 level was significantly lower in the H21.2%-S [8.3 ± 6.6 ng/ml; P = 0.01; 95% confidence interval (CI), 3.2–35.8] than in the Control-S (27.9 ± 17.0 ng/ml). The endothelial glycocalyx was significantly thicker in the H21.2%-S (0.15 ± 0.02 µm; P = 0.007; 95% CI, 0.02–0.2) than in the Control-S (0.06 ± 0.02 µm). The survival time was longer in the H21.2%-S (327 ± 67 min, P = 0.0160) than in the Control-S (246 ± 69 min). The hemoglobin level was significantly lower in the H21.2%-S (9.4 ± 0.5 g/dl; P = 0.0034; 95% CI, 0.6–2.9) than in the Control-S (11.1 ± 0.8 g/dl). However, the H23.0%-S was not significant. Conclusions Inhalation of 1.2% H2 gas protected the endothelial glycocalyx and prolonged survival time during hemorrhagic shock. Therapeutic efficacy might vary depending on the concentration.