Abstract 17002: Post-Arrest Arterial Hyper-Oxygenation and Cardiac Mitochondrial Function

TL;DRAbstract

Introduction: Post-ischemic re-oxygenation is necessary to minimize ischemic injury, but itself can induce further reperfusion injury through the induction of reactive oxygen species (ROS). Utilization of oxygen within the cell primarily occurs in the mitochondria. The objective of this study was to determine heart mitochondrial function following 1 hour of controlled arterial oxygenation following cardiac arrest and ROSC. We hypothesized that arterial hyper-oxygenation following ROSC would result in greater impairment of heart mitochondrial function. Methods: Two experimental protocols were completed using a rat KCl arrest model. In experiment 1, animals underwent a 6 min cardiac arrest and were resuscitated with standard thumper CPR, ventilation and epinephrine and then ventilated with 100% O2 (hyperoxia group) or 40% O2 (normoxia group) for 60 min. In experiment 2, animals underwent a 25 min cardiac arrest and were resuscitated with cardiopulmonary bypass. Arterial PO2 was titrated

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