Effect of naloxone after spinal cord injury in the rat - Inducible nitric oxide synthase expression, superoxide dismutase activity, and ultrastructural changes

Erman T. , GOCER A. İ. , YILDIZ M. , TUNA M. , POLAT S. , ILDAN F.

NEUROSURGERY QUARTERLY, vol.14, no.4, pp.249-256, 2004 (Journal Indexed in SCI) identifier identifier

  • Publication Type: Article / Article
  • Volume: 14 Issue: 4
  • Publication Date: 2004
  • Doi Number: 10.1097/00013414-200412000-00010
  • Page Numbers: pp.249-256


Endorphins have been implicated in the pathophysiology of spinal cord injury (SCI). Although some possible mechanisms for the therapeutic actions of naloxone have been Postulated, the exact mechanism of these favorable actions is not yet known with certainty. The benefit of naloxone in the recovery of neurologic function has generally been attributed to its action at the opiate receptors. The effect of naloxone on the inducible nitric oxide synthase (iNOS) immuno reactivity, superoxide dismutase (SOD) level, and ultrastructural findings were studied in rats at the early and late stages of SCI, produced with an aneurysm clip on the T2 to T7 segments. Severity rats were randomly allocated to 4 groups. The animals in group I (10 rats) were killed to provide normal spinal cord tissue for testing. Group 2 (20 rats) underwent 6-segment laminectomy so that the effects of total laminectomy Could be determined. Group 3 (20 rats) underwent 6-segment T2 to T7 laminectomy, and SCI was produced by extradural compression of the exposed cord. The same procedures were performed in the 20 rats in group 4, but these rats also received 1 (2 mg/kg) intraperitoneal injection of naloxone immediately after the injury, a second dose 24 hours after trauma, and a third dose 48 hours after trauma. Half of the animals from groups 3 and 4 were killed 2 hours after trauma, and the other half were killed 48 hours after trauma. The exposed cord segments were immediately removed and processed for analysis. The results showed that naloxone treatment reduces secondary structural changes in damaged rat spinal cord tissue by affecting iNOS and SOD activity.