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Journal of Biomedicine and Biotechnology
Volume 2011 (2011), Article ID 145214, 8 pages
http://dx.doi.org/10.1155/2011/145214
Research Article

Attenuation of Brain Nitrostative and Oxidative Damage by Brain Cooling during Experimental Traumatic Brain Injury

1Institute of Clinical Medicine, School of Medicine, National Cheng Kung University, Tainan 704, Taiwan
2Department of Biotechnology, Southern Taiwan University, Tainan 710, Taiwan
3Department of Surgery, Chi Mei Medical Center, Tainan 710, Taiwan
4Division of Trauma and Emergency Surgery, Chang Gung Memorial Hospital and Kaohsiung Medical Center, Kaohsiung 833, Taiwan
5Department of Medical Research, Chi Mei Medical Center, Tainan 710, Taiwan
6Graduate Institute of Disease Prevention and Control, Taipei Medical University, Taipei 112, Taiwan

Received 25 June 2010; Revised 16 December 2010; Accepted 4 January 2011

Academic Editor: Abdel A. Abdel-Rahman

Copyright © 2011 Jinn-Rung Kuo 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.

Abstract

The aim of the present study was to ascertain whether brain cooling causes attenuation of traumatic brain injury by reducing brain nitrostative and oxidative damage. Brain cooling was accomplished by infusion of 5 mL of 4°C saline over 5 minutes via the external jugular vein. Immediately after the onset of traumatic brain injury, rats were randomized into two groups and given 37°C or 4°C normal saline. Another group of rats were used as sham operated controls. Behavioral and biochemical assessments were conducted on 72 hours after brain injury or sham operation. As compared to those of the sham-operated controls, the 37°C saline-treated brain injured animals displayed motor deficits, higher cerebral contusion volume and incidence, higher oxidative damage (e.g., lower values of cerebral superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, but higher values of cerebral malondialdehyde), and higher nitrostative damage (e.g., higher values of neuronal nitric oxide synthase and 3-nitrotyrosine). All the motor deficits and brain nitrostative and oxidative damage were significantly reduced by retrograde perfusion of 4°C saline via the jugular vein. Our data suggest that brain cooling may improve the outcomes of traumatic brain injury in rats by reducing brain nitrostative and oxidative damage.