• Ryan W Morgan, Robert M Sutton, Adam S Himebauch, Anna L Roberts, William P Landis, Yuxi Lin, Jonathan Starr, Abhay Ranganathan, Nile Delso, Constantine D Mavroudis, Lindsay Volk, Julia Slovis, Alexandra M Marquez, Vinay M Nadkarni, Marco Hefti, Robert A Berg, and Todd J Kilbaugh.
• Department of Anesthesiology and Critical Care Medicine, Children's Hospital of Philadelphia, United States; Department of Anesthesiology and Critical Care Medicine, Perelman School of Medicine at the University of Pennsylvania, United States. Electronic address: morganr1@email.chop.edu.
• Resuscitation. 2021 May 1; 162: 274-283.

AimInhaled nitric oxide (iNO) during cardiopulmonary resuscitation (CPR) improved systemic hemodynamics and outcomes in a preclinical model of adult in-hospital cardiac arrest (IHCA) and may also have a neuroprotective role following cardiac arrest. The primary objectives of this study were to determine if iNO during CPR would improve cerebral hemodynamics and mitochondrial function in a pediatric model of lipopolysaccharide-induced shock-associated IHCA.MethodsAfter lipopolysaccharide infusion and ventricular fibrillation induction, 20 1-month-old piglets received hemodynamic-directed CPR and were randomized to blinded treatment with or without iNO (80 ppm) during and after CPR. Defibrillation attempts began at 10 min with a 20-min maximum CPR duration. Cerebral tissue from animals surviving 1-h post-arrest underwent high-resolution respirometry to evaluate the mitochondrial electron transport system and immunohistochemical analyses to assess neuropathology.ResultsDuring CPR, the iNO group had higher mean aortic pressure (41.6 ± 2.0 vs. 36.0 ± 1.4 mmHg; p = 0.005); diastolic BP (32.4 ± 2.4 vs. 27.1 ± 1.7 mmHg; p = 0.03); cerebral perfusion pressure (25.0 ± 2.6 vs. 19.1 ± 1.8 mmHg; p = 0.02); and cerebral blood flow relative to baseline (rCBF: 243.2 ± 54.1 vs. 115.5 ± 37.2%; p = 0.02). Among the 8/10 survivors in each group, the iNO group had higher mitochondrial Complex I oxidative phosphorylation in the cerebral cortex (3.60 [3.56, 3.99] vs. 3.23 [2.44, 3.46] pmol O2/s mg; p = 0.01) and hippocampus (4.79 [4.35, 5.18] vs. 3.17 [2.75, 4.58] pmol O2/s mg; p = 0.02). There were no other differences in mitochondrial respiration or brain injury between groups.ConclusionsTreatment with iNO during CPR resulted in superior systemic hemodynamics, rCBF, and cerebral mitochondrial Complex I respiration in this pediatric cardiac arrest model.Copyright © 2021 Elsevier B.V. All rights reserved.

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