Abstract 11607: Effects of Delayed Treatment With Inhaled Hydrogen on Oxidative Stress and Inflammatory Cytokines After Resuscitation in a Porcine Model of Cardiac Arrest

Abstract

Introduction: Immediate treatment with inhaled hydrogen (H 2 ) has been demonstrated to attenuate oxidative stress conditions and inflammatory cytokines in serum after resuscitation from cardiac arrest. However, early applying inhaled H 2 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 H 2 on oxidative stress and inflammatory cytokines in a porcine model of cardiac arrest (CA). Hypothesis: Delayed inhalation of H 2 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 H 2 (DH group) or continuous inhalation of room air (C group). DH group animals were ventilated with 2% H 2 /21% oxygen from post-resuscitation 120 min (PR120) until PR240 min. Serum levels of oxidative product (8-iso-PGF 2α ) 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-PGF 2α 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-PGF 2α 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.