Abstract 219: Supplement Oxygen Dependence of Dissociated Oxygen Metabolism From Carbon Dioxide and Oxidative Toxic Stress in Post-Cardiac Arrest

Abstract

Objective: We recently reported a dissociation of oxygen metabolism in post-cardiac arrest rodents, which was represented by an increase in oxygen consumption (VO 2 ) without a concomitant increase in carbon dioxide generation (VCO 2 ) resulting in a lowered respiratory quotient (RQ) outside of the normally cited range of 0.7-1.0. We hypothesize that high supplemental O 2 is associated with both increased dissociation of oxygen metabolism and oxidative toxic stress after cardiac arrest (CA). Methods: Rats were resuscitated from 10 minutes of asphyxial CA and stratified into 2 groups: those that inhaled 100% supplemental O 2 (CA-FIO2 1.0) and those that inhaled 30% supplemental O 2 (CA-FIO2 0.3). We prepared a sham surgery group for comparison (sham-FIO2 0.3). Our newly developed method enabled measurements of VO 2 and VCO 2 from low to high inspiratory supplemental O 2 levels. RQ was calculated as VCO 2 /VO 2 . After 2 hours, we collected urine and tissue samples to determine the degree of reactive oxygen species (ROS) generation. Results: CA increased VO 2 (28.5±8.1 mL/kg/min at FIO2 1.0 and 19.1±3.0 at FIO2 0.3, p<0.05) compared with the sham group (15.0±1.4), whereas no differences in VCO 2 were found among the three groups. RQ of CA-FIO2 1.0 animals persistently decreased to 0.57±0.03 (0.84 ±0.10 at CA-FIO2 0.3 and 0.96±0.14 at sham-FIO2 0.3). Regarding ROS generation, urinary 8-hydroxydeoxyguanosine (8-OHdG) and brain carbonyl protein of CA-FIO2 1.0 animals was significantly higher than the CA-FIO2 0.3 or sham groups. Conclusions: 100% supplemental oxygen increased VO 2 but not VCO 2 . 8-OHdG is produced during the repair of cellular DNA damaged from oxidative toxic stress and excreted into the urine. Our findings suggest that the high supplemental oxygen aggravate both dissociation of oxygen metabolism and oxidative toxic stress in post-CA rodents.