151. Effect of dimethyl fumarate on mitochondrial metabolism in a pediatric porcine model of asphyxia-induced in-hospital cardiac arrest
- Author
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Sarah Piel, Meagan J. McManus, Kristina N. Heye, Forrest Beaulieu, Hossein Fazelinia, Joanna I. Janowska, Bryce MacTurk, Jonathan Starr, Hunter Gaudio, Nisha Patel, Marco M. Hefti, Martin E. Smalley, Jordan N. Hook, Neha V. Kohli, James Bruton, Thomas Hallowell, Nile Delso, Anna Roberts, Yuxi Lin, Johannes K. Ehinger, Michael Karlsson, Robert A. Berg, Ryan W. Morgan, and Todd J. Kilbaugh
- Subjects
Cardiac arrest ,Asphyxia ,Dimethyl fumarate ,Heart ,Brain ,Metabolism ,Medicine ,Science - Abstract
Abstract Neurological and cardiac injuries are significant contributors to morbidity and mortality following pediatric in-hospital cardiac arrest (IHCA). Preservation of mitochondrial function may be critical for reducing these injuries. Dimethyl fumarate (DMF) has shown potential to enhance mitochondrial content and reduce oxidative damage. To investigate the efficacy of DMF in mitigating mitochondrial injury in a pediatric porcine model of IHCA, toddler-aged piglets were subjected to asphyxia-induced CA, followed by ventricular fibrillation, high-quality cardiopulmonary resuscitation, and random assignment to receive either DMF (30 mg/kg) or placebo for four days. Sham animals underwent similar anesthesia protocols without CA. After four days, tissues were analyzed for mitochondrial markers. In the brain, untreated CA animals exhibited a reduced expression of proteins of the oxidative phosphorylation system (CI, CIV, CV) and decreased mitochondrial respiration (p
- Published
- 2024
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