Effects of Post‐Resuscitation Normoxic Therapy on Oxygen‐Sensitive Oxidative Stress in a Rat Model of Cardiac Arrest

Background Cardiac arrest (CA) can induce oxidative stress after resuscitation, which causes cellular and organ damage. We hypothesized that post‐resuscitation normoxic therapy would protect organs against oxidative stress and improve oxygen metabolism and survival. We tested the oxygen‐sensitive reactive oxygen species from mitochondria to determine the association with hyperoxia‐induced oxidative stress. Methods and Results Sprague–Dawley rats were subjected to 10‐minute asphyxia‐induced CA with a fraction of inspired O2 of 0.3 or 1.0 (normoxia versus hyperoxia, respectively) after resuscitation. The survival rate at 48 hours was higher in the normoxia group than in the hyperoxia group (77% versus 28%, P