Date of this Version
Journal of the American Heart Association
Background Although advances in cardiopulmonary resuscitation have improved survival from cardiac arrest (CA), neurologic injury persists and impaired mitochondrial bioenergetics may be critical for targeted neuroresuscitation. The authors sought to determine if excellent cardiopulmonary resuscitation and postresuscitation care and good traditional survival rates result in persistently disordered cerebral mitochondrial bioenergetics in a porcine pediatric model of asphyxia‐associated ventricular fibrillation CA.
Methods and Results After 7 minutes of asphyxia, followed by ventricular fibrillation, 5 female 1‐month‐old swine (4 sham) received blood pressure–targeted care: titration of compression depth to systolic blood pressure of 90 mm Hg and vasopressor administration to a coronary perfusion pressure >20 mm Hg. All animals received protocol‐based vasopressor support after return of spontaneous circulation for 4 hours before they were killed. The primary outcome was integrated mitochondrial electron transport system (ETS) function. CA animals displayed significantly decreased maximal, coupled oxidative phosphorylating respiration (OXPHOSCI+CII) in cortex (PPPPCI PCII PCIPCII PCI+CII), as well as a 30% reduction in citrate synthase activity (P<0.04).
Conclusions Mitochondria in both the cortex and hippocampus displayed significant alterations in respiratory function after CA despite excellent cardiopulmonary resuscitation and postresuscitation care in asphyxia‐associated ventricular fibrillation CA. Analysis of integrated ETS function identifies mitochondrial bioenergetic failure as a target for goal‐directed neuroresuscitation after CA. IACUC Protocol: IAC 13‐001023.
© 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
acute brain injury, brain, cardiac arrest, electron transport system, mitochondria, neuroprotection
Kilbaugh, T., Sutton, R. M., Karlsson, M., Hansson, M. J., Naim, M. Y., Morgan, R. W., Bratinov, G., Lampe, J., Nadkarni, V., Becker, L., Margulies, S. S., & Berg, R. A. (2015). Persistently Altered Brain Mitochondrial Bioenergetics After Apparently Successful Resuscitation From Cardiac Arrest. Journal of the American Heart Association, 4 (9), e002232-. http://dx.doi.org/10.1161/JAHA.115.002232
Date Posted: 25 May 2016
This document has been peer reviewed.