Hydrogen Gas Protects Hearts from Heart Attack Damage in Rats
- Authors
- Hongxiao Yang, Shuang Liu, Huijun Du, Zi Hong, Yajing Lv, Chaoqun Nie, Wei Yang, Yunan Gao
- Journal
- International Journal of Medical Sciences
- Year
- 2021
- DOI
- 10.7150/ijms.61329
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Acute Myocardial Infarction
- Body System
- Cardiovascular
TL;DR
Breathing in hydrogen gas helped improve heart function and reduce heart damage in rats after a heart attack by lowering inflammation and oxidative stress.
Key Finding
Hydrogen gas inhalation reduced heart damage and improved heart function in rats with acute heart attacks by decreasing oxidative stress (cellular damage from unstable molecules) and reducing inflammation in heart cells.
Summary
This rat study tested whether inhaling hydrogen gas could reduce heart damage from a heart attack. Researchers blocked blood flow to the heart in rats and then gave some of them hydrogen gas to breathe for 24 hours. Rats that received hydrogen showed better heart function, smaller areas of dead heart tissue, less inflammation, and lower levels of damage markers in their blood compared to rats that didn't receive hydrogen.
Practical Takeaway
While this rat study suggests hydrogen gas may protect heart tissue during a heart attack, it is early-stage research that has not been tested in humans. The findings are promising but cannot yet be applied to human heart attack treatment without further clinical trials.
Abstract
Purpose: Hydrogen (H2) is an antioxidant with anti-inflammatory and apoptosis functions.This study aimed to estimate the effects of H2 on acute myocardial infarction (AMI) in rats and its association with the inhibition of oxidative stress and cardiomyocyte pyroptosis. Methods: Sixty-four rats were randomly divided into three groups (Sham, AMI, and H2). The left anterior descending coronary artery (LAD) of rats in the AMI and H2 groups was ligated, while rats in the Sham group were threaded without ligation. In addition, 2% H2 was administered by inhalation for 24 h after ligation in the H2 group. Transthoracic echocardiography was performed after H2 inhalation, followed by collection of the serum and cardiac tissue of all rats. Results: H2 inhalation ameliorated the cardiac dysfunction, infarct size and inflammatory cell infiltration caused by AMI. Meanwhile, H2 inhalation reduced the concentration of serum Troponin I (TnI), brain natriuretic peptide (BNP), reactive oxygen species (ROS), cardiac malondialdehyde (MDA), and 8-OHdG. In addition, H2 inhalation inhibited cardiac inflammation and pyroptosis relative proteins expression. Conclusion: H2 effectively promoted heart functions in AMI rats by regulating oxidative stress and pyroptosis.