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BioMed Research International
Volume 2014, Article ID 192769, 9 pages
Research Article

Impaired Cerebral Mitochondrial Oxidative Phosphorylation Function in a Rat Model of Ventricular Fibrillation and Cardiopulmonary Resuscitation

1Department of Emergency Medicine, The First People’s Hospital of Foshan, 81 Ling Nan Road, Foshan, Guangdong 528000, China
2Institute of Cardiopulmonary Cerebral Resuscitation, Sun Yat-sen University, 107 Yan Jiang Xi Road, Guangzhou, Guangdong 510120, China
3Department of Emergency Medicine, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, 107 Yan Jiang Xi Road, Guangzhou, Guangdong 510120, China

Received 1 November 2013; Accepted 4 January 2014; Published 18 February 2014

Academic Editor: Giuseppe Ristagno

Copyright © 2014 Jun Jiang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Postcardiac arrest brain injury significantly contributes to mortality and morbidity in patients suffering from cardiac arrest (CA). Evidence that shows that mitochondrial dysfunction appears to be a key factor in tissue damage after ischemia/reperfusion is accumulating. However, limited data are available regarding the cerebral mitochondrial dysfunction during CA and cardiopulmonary resuscitation (CPR) and its relationship to the alterations of high-energy phosphate. Here, we sought to identify alterations of mitochondrial morphology and oxidative phosphorylation function as well as high-energy phosphates during CA and CPR in a rat model of ventricular fibrillation (VF). We found that impairment of mitochondrial respiration and partial depletion of adenosine triphosphate (ATP) and phosphocreatine (PCr) developed in the cerebral cortex and hippocampus following a prolonged cardiac arrest. Optimal CPR might ameliorate the deranged phosphorus metabolism and preserve mitochondrial function. No obvious ultrastructural abnormalities of mitochondria have been found during CA. We conclude that CA causes cerebral mitochondrial dysfunction along with decay of high-energy phosphates, which would be mitigated with CPR. This study may broaden our understanding of the pathogenic processes underlying global cerebral ischemic injury and provide a potential therapeutic strategy that aimed at preserving cerebral mitochondrial function during CA.