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Post-cardiac arrest brain injury significantly contributes to mortality and morbidity in patients suffering from cardiac arrest (CA).Evidence is accumulating that shows that mitochondrial dysfunction appears to be a key factor in tissue damage after ischemia/reperfusion.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 ofventricular 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 aimed at preservation of cerebral mitochondrial function during CA.