Abstract 11607: Effects of Delayed Treatment With Inhaled Hydrogen on Oxidative Stress and Inflammatory Cytokines After Resuscitation in a Porcine Model of Cardiac Arrest
Introduction: Immediate treatment with inhaled hydrogen (H2) has been demonstrated to attenuate oxidative stress conditions and inflammatory cytokines in serum after resuscitation from cardiac arrest. However, early applying inhaled H2 is not practical especially in out of hospital cardiac arrest because of the safety issue. In the present study, we investigated the effects of delayed treatment with H2 on oxidative stress and inflammatory cytokines in a porcine model of cardiac arrest (CA).
Hypothesis: Delayed inhalation of H2 reduces proinflammatory cytokines but without effect on oxidative stress after resuscitation in a CA porcine model.
Methods: Twenty male domestic pigs weighing 39±2 kg were studied. Ventricular fibrillation (VF) was induced electrically and CPR was initiated after 10 min of untreated VF. Animals were randomized into two groups immediately after successfully resuscitation: delayed inhalation of H2 (DH group) or continuous inhalation of room air (C group). DH group animals were ventilated with 2% H2/21% oxygen from post-resuscitation 120 min (PR120) until PR240 min. Serum levels of oxidative product (8-iso-PGF2α) and proinflammatory cytokines (tumor necrosis factor-α [TNF-α], interleukin-6 [IL-6], and high-mobility group box protein 1 [HMGB1]) were measured by ELISA at baseline (BL), PR30, PR180 and PR360.
Results: Serum levels of 8-iso-PGF2α in all the animals were significantly increased at PR30 then decreased to the levels of BL after PR180. The levels of TNF-α, IL-6 and HMGB1 in serum of all animals were elevated after PR180. Although no significant differences in the levels of 8-iso-PGF2α were observed between both groups, the levels of TNF-α, IL-6 and HMGB1 were significantly lower in DH group animals when compared with those in C group (Figure).
Conclusions: Delayed treatment with H2 attenuates proinflammatory cytokines but without effect on oxidative stress conditions after resuscitation.
Author Disclosures: Z. Yang: None. T. Yu: None. C. Wen: None. X. Zhai: None. M. Peberdy: None. J. Ornato: None. W. Tang: None.
- © 2016 by American Heart Association, Inc.