The effect of epidural cooling on lipid peroxidation after experimental spinal cord injury
- PMID: 9773452
- DOI: 10.1038/sj.sc.3100660
The effect of epidural cooling on lipid peroxidation after experimental spinal cord injury
Abstract
Study design: The effect of epidural space perfusion with chilled saline solution (% 0.9 NaCl) on lipid peroxidation after experimental spinal cord injury in rats was evaluated.
Objectives: The extent of lipid peroxidation is a useful parameter for evaluating the cellular disturbance caused by spinal cord trauma in experimental conditions. The protective effects of hypothermia against neurological injury resulting from trauma or ischemia both in experimental and clinical situations have been demonstrated.
Setting: Departments of Neurosurgery and Biochemistry, Cerrahpaşa Medical School, Istanbul, Turkey.
Methods: Twenty-five female Wistar Albino rats were used. There were five rats in group I (sham-operated), seven rats in group II (trauma), and eight rats in group III (epidural cooling). The remaining five rats were used for the pilot study to determine the spinal cord and body temperature. A clip compression method was used to produce acute spinal cord injury. In group III, 30 min after the trauma the injured spinal cord was cooled by perfusion of the epidural space with chilled saline solution (% 0.9 NaCl) with a flow rate of 5 ml/min for 30 min. At 2 h after trauma, all rats other than the ones used in the pilot study, were sacrificed and the spinal cords were excised. The extent of lipid peroxidation in the spinal cord was assessed by measuring the tissue content of malonil dialdehyde (MDA).
Results: The tissue MDA contents were 1.58 micromol MDA/gram wet weight (gww) in group I (sham-operated), 2.58 micromol MDA/gww in group 2 (trauma), and 1.77 micromol/gww in group 3 (epidural cooling), the differences being statistically significant.
Conclusion: The results indicated that epidural cooling of traumatized spinal cord is effective in preventing secondary damage due to the peroxidation of lipid membranes.
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