Inhaled Nitric Oxide Improves Cerebral Mitochondrial Function In A Blinded, Randomized Controlled Pediatric Swine Asphyxial Cardiac Arrest Trial

Introduction: Neurologic injury following pediatric cardiac arrest (CA) remains common. Inhaled nitric oxide (iNO) may mitigate cerebral mitochondrial dysfunction, a critical convergence point for secondary brain injury, triggered by CA. Hypothesis: Following asphyxia and cardiac arrest, animals treated with 20ppm iNO during CPR and four hours post-return of spontaneous circulation (ROSC) will have improved cerebral blood flow (CBF) and improved mitochondrial function as defined by increased respiratory control ratio (RCR) and decreased mitochondrial reactive oxygen species (mtROS) compared with placebo. Methods: Model: 4-week-old swine received 7 minutes of asphyxia, then ventricular fibrillation. Guideline CPR: compression depth (CD) ≥1/3 of the chest diameter and standard epinephrine continued for 10 mins or until ROSC, with protocolized post-ROSC care. In a blinded fashion, subjects were randomized (iNO 20 ppm initiated 1 minute into CPR period, n=10, or placebo, n=10). Shams (n=4) did not undergo CA ...