Hydrogen gas inhalation alleviates oxidative stress in patients with post-cardiac arrest syndrome.

Abstract

Post-cardiac arrest syndrome involves pronounced oxidative stress as a central pathophysiological feature. This pilot study enrolled five comatose patients following cardiac arrest (three male; mean age 65 ± 15 years; four cardiogenic, one septic origin) who received 2% hydrogen gas inhalation with titrated oxygen for 18 hours alongside target temperature management. Blood hydrogen concentrations were measurable and equilibrated with inhaled levels. Oxidative stress markers—including derivatives of reactive oxygen metabolites, biological antioxidant potential, 8-hydroxy-2'-deoxyguanosine, hexanoyl-lysine, and lipid hydroperoxide—as well as interleukin-6 and tumor necrosis factor-α were assessed at baseline and at 3, 9, 18, and 24 hours post-inhalation. Among cardiogenic cases, oxidative stress indices declined, whereas cytokine levels remained stable. In the single septic case, cytokine levels fell but oxidative stress markers did not change appreciably. The authors note that methodological constraints preclude definitive conclusions regarding hydrogen's effects in this population.

Mechanism

Inhaled molecular hydrogen is thought to selectively scavenge reactive oxygen species, thereby reducing circulating oxidative stress markers such as reactive oxygen metabolite derivatives and 8-hydroxy-2'-deoxyguanosine, particularly in cardiogenic post-cardiac arrest cases.