Hydrogen Gas Helps Heart Recovery After Cardiac Arrest in Rats
- Authors
- Xiaohui Gong, Xinhui Fan, Xinxin Yin, Tonghui Xu, Jiaxin Li, Jialin Guo, Xiangkai Zhao, Shujian Wei, Qiuhuan Yuan, Jiali Wang, Xuchen Han, Yuguo Chen
- Journal
- Experimental and Therapeutic Medicine
- Year
- 2022
- DOI
- 10.3892/etm.2022.11302
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Cardiac Arrest
- Body System
- Cardiovascular
TL;DR
Breathing in hydrogen gas after a heart attack and CPR can help improve heart function and survival by reducing harmful cell processes in rats.
Key Finding
Rats treated with hydrogen gas after cardiac arrest and resuscitation showed improved survival rates and better heart function, with less damage to heart muscle cells compared to untreated rats.
Summary
Researchers tested whether hydrogen gas therapy could protect the heart after cardiac arrest and resuscitation in rats. Rats that received 2% hydrogen gas to breathe after being revived from cardiac arrest showed better survival rates and improved heart function compared to control rats. The study suggests hydrogen gas works by reducing a cellular process called autophagy (where cells break down their own components), which appears to cause damage to heart muscle cells after resuscitation.
Practical Takeaway
This is an early-stage animal study that suggests hydrogen gas inhalation may help protect heart tissue after cardiac arrest, but it does not yet demonstrate safety or effectiveness in humans. Much more research, including human clinical trials, would be needed before this approach could be considered for medical use in cardiac arrest patients.
Abstract
Hydrogen (H2) therapy is a therapeutic strategy using molecular H2. Due to its ability to regulate cell homeostasis, H2 therapy has exhibited marked therapeutic effects on a number of oxidative stress-associated diseases. The present study investigated the effectiveness of H2 therapy in protecting against myocardial injury in a rat model of asphyxial cardiac arrest and cardiopulmonary resuscitation. Rats underwent 10-min asphyxia-induced cardiac arrest (CA) and cardiopulmonary resuscitation (CPR), and were randomly divided into control and H2 therapy groups. After resuscitation, the H2 therapy group was administered room air mixed with 2% H2 gas for respiration. During CA/CPR, the arterial pressure and heart rate were measured every minute. Survival rate, cardiac function, myocardial injury biomarkers creatine kinase-MB and cardiac troponin-T, and histopathological changes were evaluated to determine the protective effects of H2 therapy in CA/CPR. Immunohistochemistry and western blot analysis were used to determine the expression levels of autophagy-associated proteins. In vitro, H9C2 cells were subjected to hypoxia/reoxygenation and H2-rich medium was used in H2 treatment groups. Western blotting and immunofluorescence were used to observe the expression levels of autophagy-associated proteins. Moreover, an adenovirus-monomeric red fluorescent protein-green fluorescent protein-LC3 construct was used to explore the dynamics of autophagy in the H9C2 cells. The results showed that H2 therapy significantly improved post-resuscitation survival and cardiac function. H2 therapy also improved mitochondrial mass and decreased autophagosome numbers in cardiomyocytes after resuscitation. The treatment inhibited autophagy activation, with lower expression levels of autophagy-associated proteins and decreased autophagosome formation in vivo and vitro. In conclusion, H2 gas inhalation after return of spontaneous circulation improved cardiac function via the inhibition of autophagy.