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BioMed Research International
Volume 2017 (2017), Article ID 1948070, 9 pages
Research Article

Dynamic Changes of Mitochondrial Fusion and Fission in Brain Injury after Cardiac Arrest in Rats

1Department of Emergency Medicine, The First Affiliated Hospital of Soochow University, Soochow, China
2Institute of Cardiopulmonary Cerebral Resuscitation, Sun Yat-sen University, Guangzhou, China
3Department of Clinical Laboratory Center, The First Affiliated Hospital of Soochow University, Soochow, China
4Department of Emergency Medicine, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China

Correspondence should be addressed to Peng Wang and Zitong Huang

Received 17 August 2017; Revised 2 December 2017; Accepted 7 December 2017; Published 28 December 2017

Academic Editor: Sergio Claudio Saccà

Copyright © 2017 Yi Li 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.


Mitochondria change their morphology dynamically by continual fusion and fission processes to fulfill their function. However, little is known about the effect of cardiac arrest on mitochondrial dynamics. This study aimed to investigate time-dependent change of the mitochondrial dynamics after brain ischemic injury in rats of cardiac arrest. After resuscitation, obvious neuronal injury, reduced adenosine triphosphate (ATP) levels, excessive reactive oxygen species (ROS) generation, decreased mitochondrial membrane potential (MMP), and increased release of mitochondrial cytochrome c were observed at 12 h and 24 h after cardiac arrest. Moreover, we found that elongation of mitochondria was observed at 4 h after cardiac arrest, whereas fragmented mitochondria were significantly increased, along with concomitant increase in the fission proteins Drp1 and Fis1 and a reduction in the fusion proteins Mfn1 and Mfn2 at 12 h and 24 h after cardiac arrest. Taken together, these findings suggest that imbalance in mitochondrial dynamics probably contributes to brain injury after cardiac arrest.