Abstract 14096: Ischemic Postconditioning During Cardiopulmonary Resuscitation Normalizes Mitochondrial Function in a Porcine Model of Prolonged Cardiac Arrest

Introduction: Mitochondrial dysfunction is a hallmark of prolonged ischemia, however it’s onset during cardiac arrest (CA) and reperfusion with cardiopulmonary resuscitation (CPR) has yet to be elucidated. In a porcine model of CA, ischemic postconditioning (IPC) during CPR increased neurologically intact survival. We hypothesized that reperfusion injury, as evidenced by mitochondrial dysfunction, develops during CPR and is rescued with IPC. We investigated the effect of CA, CPR, and IPC on mitochondrial function and viability. Methods: After 15 min of ventricular fibrillation, 30 animals were randomized to no CPR (VF, n=10), active compression decompression + impedance threshold device (ACD-ITD) CPR (Control, n=9), or ACD-ITD CPR + IPC (IPC, n=11). Aortic blood pressure and ECG were continuously recorded. IPC consisted of 3 cycles of 20 sec compression / 20 sec pause for the first 2 min of CPR. Cardiac mitochondria were isolated via differential centrifugation 4 min after initiation of CPR. Additionally,...