Oxidative stress plays a key role in the pathophysiology of
post-cardiac arrest syndrome. Molecular
hydrogen reduces oxidative stress and exerts anti-inflammatory effects in an animal model of
cardiac arrest. However, its effect on human
post-cardiac arrest syndrome is unclear. We consecutively enrolled five
comatose post-
cardiac arrest patients (three males; mean age, 65 ± 15 years; four cardiogenic, one septic
cardiac arrest) and evaluated temporal changes in oxidative stress markers and
cytokines with inhaled
hydrogen. All patients were treated with target temperature management.
Hydrogen gas inhalation (2%
hydrogen with titrated
oxygen) was initiated upon admission for 18 h. Blood
hydrogen concentrations, plasma and urine oxidative stress markers (derivatives of reactive
oxygen metabolites,
biological antioxidant potential,
8-hydroxy-2'-deoxyguanosine, N ɛ-hexanoyl-
lysine,
lipid hydroperoxide), and
cytokines (
interleukin-6 and
tumor necrosis factor-α) were measured before and 3, 9, 18, and 24 h after
hydrogen gas inhalation. Arterial
hydrogen concentration was measurable and it was equilibrated with inhaled
hydrogen. Oxidative stress was reduced and
cytokine levels were unchanged in cardiogenic patients, whereas oxidative stress was unchanged and
cytokine levels were diminished in the septic patient. The effect of inhaled
hydrogen on oxidative stress and
cytokines in
comatose post-
cardiac arrest patients remains indefinite because of methodological weaknesses.