Hydrogen Gas Cuts Heart Attack Damage by 53% in Dog Study
- Authors
- Akemi Yoshida, Hiroshi Asanuma, Hideyuki Sasaki, Shoji Sanada, Satoru Yamazaki, Yoshihiro Asano, Yoshiro Shinozaki, Hidezo Mori, Akito Shimouchi, Motoaki Sano, Masanori Asakura, Tetsuo Minamino, Seiji Takashima, Masaru Sugimachi, Naoki Mochizuki, Masafumi Kitakaze
- Journal
- Cardiovascular Drugs and Therapy
- Year
- 2012
- DOI
- 10.1007/s10557-012-6381-5
- Study Type
- Dog
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Acute Myocardial Infarction
- Body System
- Cardiovascular
TL;DR
Breathing in hydrogen gas can significantly reduce heart damage after a heart attack in dogs by affecting certain cell functions.
Key Finding
Inhaling hydrogen gas reduced heart damage by approximately 53% in dogs experiencing simulated heart attack and blood flow restoration, working through activation of specific mitochondrial channels rather than through antioxidant mechanisms.
Summary
Researchers tested whether inhaling hydrogen gas could protect dog hearts from damage during a heart attack and subsequent blood flow restoration. They found that hydrogen gas inhalation reduced heart damage by about half, and this protection worked through a specific mechanism involving channels in the heart's energy-producing structures (mitochondria). Importantly, blocking these channels eliminated hydrogen's protective effect, suggesting this is how hydrogen provides its benefit.
Practical Takeaway
This dog study provides early evidence that hydrogen gas may protect heart tissue during ischemia-reperfusion injury through a specific cellular mechanism. However, this is a single animal study in a controlled laboratory setting; human trials would be needed to determine if these results apply to people with actual heart attacks. The findings suggest a potential direction for future research but do not yet support any clinical recommendations.
Abstract
Inhalation of hydrogen (H(2)) gas has been shown to limit infarct size following ischemia-reperfusion injury in rat hearts. However, H(2) gas-induced cardioprotection has not been tested in large animals and the precise cellular mechanism of protection has not been elucidated. We investigated whether opening of mitochondrial ATP-sensitive K+ channels (mK(ATP)) and subsequent inhibition of mitochondrial permeability transition pores (mPTP) mediates the infarct size-limiting effect of H(2) gas in canine hearts. The left anterior descending coronary artery of beagle dogs was occluded for 90 min followed by reperfusion for 6 h. Either 1.3% H(2) or control gas was inhaled from 10 min prior to start of reperfusion until 1 h of reperfusion, in the presence or absence of either 5-hydroxydecanoate (5-HD; a selective mK(ATP) blocker), or atractyloside (Atr; a mPTP opener). Systemic hemodynamic parameters did not differ among the groups. Nevertheless, H(2) gas inhalation reduced infarct size normalized by risk area (20.6±2.8% vs. control gas 44.0±2.0%; p<0.001), and administration of either 5-HD or Atr abolished the infarct size-limiting effect of H(2) gas (42.0±2.2% with 5-HD and 45.1±2.7% with Atr; both p<0.001 vs. H(2) group). Neither Atr nor 5-HD affected infarct size per se. Among all groups, NAD content and the number of apoptotic and 8-OHdG positive cells was not significantly different, indicating that the cardioprotection afforded by H(2) was not due to anti-oxidative actions or effects on the NADH dehydrogenase pathway. Inhalation of H(2) gas reduces infarct size in canine hearts via opening of mitochondrial K(ATP) channels followed by inhibition of mPTP. H(2) gas may provide an effective adjunct strategy in patients with acute myocardial infarction receiving reperfusion therapy.