Hydrogen Gas Protects Heart from Sleep Apnea Damage in Rat Study

Authors
Journal
Oxidative Medicine and Cellular Longevity
Year
DOI
10.1155/2019/7415212
Study Type
Rat
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Obstructive Sleep Apnea
Body System
Cardiovascular

TL;DR

Inhaling a hydrogen-oxygen gas mixture significantly reduced heart damage in rats with sleep apnea by decreasing stress in heart cells and lowering harmful oxygen-related molecules.

Key Finding

A hydrogen-oxygen gas mixture improved cardiac dysfunction and reduced heart tissue damage in rats exposed to chronic low-oxygen conditions similar to obstructive sleep apnea.

Summary

This study used rats to model obstructive sleep apnea (a condition where breathing repeatedly stops during sleep), which causes the heart to be exposed to low oxygen levels. Researchers gave some rats a mixture of hydrogen and oxygen gas to breathe for 35 days and found that this treatment improved heart function and reduced damage to heart tissue. The treatment appeared to work by reducing harmful molecules called reactive oxygen species and preventing cells from dying through a process called apoptosis (programmed cell death).

Practical Takeaway

This is an early-stage animal study suggesting hydrogen gas may help protect the heart from damage caused by repeated oxygen drops. However, this was only tested in rats, not humans, so it's unclear whether these results would apply to people with sleep apnea. Much more research, including human studies, would be needed before hydrogen therapy could be considered a treatment option.

Abstract

Obstructive sleep apnea (OSA) can cause intermittent changes in blood oxygen saturation, resulting in the generation of many reactive oxygen species (ROS). To discover new antioxidants and clarify the endoplasmic reticulum (ER) stress involved in cardiac injury in OSA, we established a chronic intermittent hypoxia (CIH) rat model with a fraction of inspired O2 (FiO2) ranging from 21% to 9%, 20 times/h for 8 h/day, and the rats were treated with H2-O2 mixture (67% hydrogen and 33% oxygen) for 2 h/day for 35 days. Our results showed that H2-O2 mixture remarkably improved cardiac dysfunction and myocardial fibrosis. We found that H2-O2 mixture inhalation declined ER stress-induced apoptosis via three major response pathways: PERK-eIF2α-ATF4, IRE 1-XBP1, and ATF 6. Furthermore, we revealed that H2-O2 mixture blocked c-Jun N-terminal kinase- (JNK-) MAPK activation, increased the ratio of Bcl-2/Bax, and inhibited caspase 3 cleavage to protect against CIH-induced cardiac apoptosis. In addition, H2-O2 mixture considerably decreased ROS levels via upregulating superoxide dismutase (SOD) and glutathione (GSH) as well as downregulating NADPH oxidase (NOX 2) expression in the hearts of CIH rats. All the results demonstrated that H2-O2 mixture significantly reduced ER stress and apoptosis and that H2 might be an efficient antioxidant against the oxidative stress injury induced by CIH.