![](/images/graphics-bg.png)
Impaired Cerebral Mitochondrial Oxidative Phosphorylation Function in a Rat Model of Ventricular Fibrillation and Cardiopulmonary Resuscitation
Joint Authors
Xu, Wen
Jiang, Longyuan
Fu, Yue
Huang, Zitong
Jiang, Jun
Fang, Xiangshao
Source
Issue
Vol. 2014, Issue 2014 (31 Dec. 2014), pp.1-9, 9 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2014-02-18
Country of Publication
Egypt
No. of Pages
9
Main Subjects
Abstract EN
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.
American Psychological Association (APA)
Jiang, Jun& Fang, Xiangshao& Fu, Yue& Xu, Wen& Jiang, Longyuan& Huang, Zitong. 2014. Impaired Cerebral Mitochondrial Oxidative Phosphorylation Function in a Rat Model of Ventricular Fibrillation and Cardiopulmonary Resuscitation. BioMed Research International،Vol. 2014, no. 2014, pp.1-9.
https://search.emarefa.net/detail/BIM-453351
Modern Language Association (MLA)
Jiang, Jun…[et al.]. Impaired Cerebral Mitochondrial Oxidative Phosphorylation Function in a Rat Model of Ventricular Fibrillation and Cardiopulmonary Resuscitation. BioMed Research International No. 2014 (2014), pp.1-9.
https://search.emarefa.net/detail/BIM-453351
American Medical Association (AMA)
Jiang, Jun& Fang, Xiangshao& Fu, Yue& Xu, Wen& Jiang, Longyuan& Huang, Zitong. Impaired Cerebral Mitochondrial Oxidative Phosphorylation Function in a Rat Model of Ventricular Fibrillation and Cardiopulmonary Resuscitation. BioMed Research International. 2014. Vol. 2014, no. 2014, pp.1-9.
https://search.emarefa.net/detail/BIM-453351
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-453351