Durk Pearson & Sandy Shaw’s®
Life Extension NewsTM
Volume 16 No. 4 • April 2013

Hydrogen Gas Protects Beagle Dog Hearts from
Ischemia-Reperfusion Injury-Induced Infarction

Researchers investigated a possible mechanism to explain how the inhalation of hydrogen gas following ischemia-reperfusion injury in rat hearts limits the infarct size.1 Noting that the effect of hydrogen on such heart injury in large animals has not been studied, they focused their study on beagle dogs that had the left anterior descending coronary artery occluded for 90 minutes, followed by reperfusion for 6 hours. The animals were treated with either 1.3% hydrogen or control gas (70% nitrogen and 30% oxygen) ten minutes prior to reperfusion until 1 hour of reperfusion had taken place.

The area of killed heart cells (infarct) was reduced by hydrogen gas as compared to control gas (and normalized by risk area) 20.6 ± 2.8% vs. 44.0 ± 2%; p<0.001. (In other words, the area at risk due to the occlusion following by reperfusion was reduced by 20.6 ± 2.8% by the hydrogen gas treatment as compared to 44.0 ± 2% by the control gas treatment.) They also identified the opening of mitochondrial K-ATP channels followed by inhibition of the mitochondrial permeability transition pores as accompanying the protective effects of limiting ischemia-reperfusion-induced infarct. The authors note that “recent accumulated evidence regarding cardioprotection afforded by ischemic pre- or post-conditioning has culminated in the idea that opening of mitochondrial ATP-sensitive K+ channels followed by inhibition of mitochondrial permeability transition pores plays a central role in limiting infarct size.”1

The researchers used drugs that prevent the opening of the mitochondrial K-ATP channel as a way to test whether the protective effects of hydrogen gas was mediated by the opening of these channels. The administration of either of two such drugs abolished the infarct size-limiting effect of hydrogen gas.

The researchers also observed that inhalation of hydrogen gas tended to reduce the incidence of lethal ventricular arrhythmia, although they did not investigate the mechanisms responsible for that.


  1. Yoshida et al. H2 mediates cardioprotection via involvements of K-ATP channels and permeability transition pores of mitochondria in dogs. Cardiovasc Drugs Ther. 26:217-226 (2012).

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