Hydrogen Gas Boosts Survival After Cardiac Arrest in Animal Study
- Authors
- Tai Yin, Lance B. Becker, Rishabh C. Choudhary, Ryosuke Takegawa, Muhammad Shoaib, Koichiro Shinozaki, Yusuke Endo, Koichiro Homma, Daniel M. Rolston, Shuhei Eguchi, Tadashi Ariyoshi, Asami Matsumoto, Kentaro Oka, Motomichi Takahashi, Tomoaki Aoki, Santiago J. Miyara, Mitsuaki Nishikimi, Junichi Sasaki, Junhwan Kim, Ernesto P. Molmenti, Kei Hayashida
- Journal
- Journal of Translational Medicine
- Year
- 2021
- DOI
- 10.1186/s12967-021-03129-1
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- United States
- Health Condition
- Cardiac Arrest
- Body System
- Cardiovascular
TL;DR
In a rat study, inhaling hydrogen gas during a specialized heart-lung resuscitation procedure improved survival rates and brain function after cardiac arrest.
Key Finding
Rats treated with hydrogen gas combined with ECMO life-support had a 77.8% survival rate compared to 22.2% in the control group, and all hydrogen-treated animals recovered brain electrical activity while none in the control group did.
Summary
Researchers studied whether adding hydrogen gas to a life-support machine (ECMO) could help rats survive cardiac arrest. Rats were given 20 minutes without oxygen to simulate cardiac arrest, then treated with either the ECMO machine alone or ECMO plus hydrogen gas. The hydrogen gas group had much higher survival rates and showed better brain electrical activity recovery, possibly because hydrogen reduced damage to blood vessel linings and excessive inflammation caused by the ECMO machine.
Practical Takeaway
This rat study suggests hydrogen gas may help protect the body during extreme medical emergencies involving life-support machines, but these results cannot yet be applied to humans. Much more research, including human clinical trials, would be needed before hydrogen could be considered as a treatment for cardiac arrest patients. The findings are promising but very early-stage.
Abstract
Background: Despite the benefits of extracorporeal cardiopulmonary resuscitation (ECPR) in cohorts of selected patients with cardiac arrest (CA), extracorporeal membrane oxygenation (ECMO) includes an artificial oxygenation membrane and circuits that contact the circulating blood and induce excessive oxidative stress and inflammatory responses, resulting in coagulopathy and endothelial cell damage. There is currently no pharmacological treatment that has been proven to improve outcomes after CA/ECPR. We aimed to test the hypothesis that administration of hydrogen gas (H2) combined with ECPR could improve outcomes after CA/ECPR in rats. Methods: Rats were subjected to 20 min of asphyxial CA and were resuscitated by ECPR. Mechanical ventilation (MV) was initiated at the beginning of ECPR. Animals were randomly assigned to the placebo or H2 gas treatment groups. The supplement gas was administered with O2 through the ECMO membrane and MV. Survival time, electroencephalography (EEG), brain functional status, and brain tissue oxygenation were measured. Changes in the plasma levels of syndecan-1 (a marker of endothelial damage), multiple cytokines, chemokines, and metabolites were also evaluated. Results: The survival rate at 4 h was 77.8% (7 out of 9) in the H2 group and 22.2% (2 out of 9) in the placebo group. The Kaplan-Meier analysis showed that H2 significantly improved the 4 h-survival endpoint (log-rank P = 0.025 vs. placebo). All animals treated with H2 regained EEG activity, whereas no recovery was observed in animals treated with placebo. H2 therapy markedly improved intra-resuscitation brain tissue oxygenation and prevented an increase in central venous pressure after ECPR. H2 attenuated an increase in syndecan-1 levels and enhanced an increase in interleukin-10, vascular endothelial growth factor, and leptin levels after ECPR. Metabolomics analysis identified significant changes at 2 h after CA/ECPR between the two groups, particularly in D-glutamine and D-glutamate metabolism. Conclusions: H2 therapy improved mortality in highly lethal CA rats rescued by ECPR and helped recover brain electrical activity. The underlying mechanism might be linked to protective effects against endothelial damage. Further studies are warranted to elucidate the mechanisms responsible for the beneficial effects of H2 on ischemia-reperfusion injury in critically ill patients who require ECMO support.