A study of adenosine treatment in experimental acute spinal cord injury. Effect on arachidonic acid metabolites

• Published in: Spine (Philadelphia, Pa. 1976) Pa. 1976), 1999-01, Vol.24 (2), p.128-132
• Main Authors: Akpek, E A, Bulutçu, E, Alanay, A, Korkusuz, P, Acaroğlu, E, Kilinç, K, Ors, U
• Format: Article
• Language: English
• Subjects: Acute Disease; Adenosine - metabolism; Adenosine - therapeutic use; Animals; Arachidonic Acid - metabolism; Dinoprostone - metabolism; Disease Models, Animal; Laminectomy; Leukotriene C4 - metabolism; Lipid Peroxidation; Male; Myelin Sheath - pathology; Nerve Compression Syndromes - drug therapy; Nerve Compression Syndromes - prevention & control; Random Allocation; Rats; Rats, Wistar; Spinal Cord - drug effects; Spinal Cord - metabolism; Spinal Cord - pathology; Spinal Cord Injuries - drug therapy; Spinal Cord Injuries - metabolism; Vasodilator Agents - metabolism; Vasodilator Agents - therapeutic use
• ISSN: 0362-2436
• DOI: 10.1097/00007632-199901150-00006

A prospective, randomized, blinded experimental trauma study. The effect of adenosine on arachidonic acid metabolites and lipid peroxidation was investigated in induced spinal cord injury. Effects of adenosine in ischemia-reperfusion models have been studied, but no studies of adenosine's effect on direct trauma to the spinal cord have been reported. Thirty-seven adult Wistar albino rats were randomly divided into four groups and underwent laminectomy. Group 1 underwent a sham operation. Group 2 received an intravenous adenosine infusion of 100 micrograms/kg per minute for 30 minutes. In Group 3, a standard spinal cord trauma of 50 g.cm strength was established at the lower thoracic level with a "weight-drop" technique, and Group 4 received an infusion of adenosine (100 micrograms/kg per minute) for 30 minutes after the trauma. Tissue prostaglandin E2 activity was significantly higher in adenosine-treated trauma groups when compared with that in other groups (P < 0.0001). The difference in tissue leukotriene C4 activity between control and trauma groups was significant (P < 0.05). Adenosine infusion after trauma limited the increases in lipid peroxidation, with the difference approaching significance at P = 0.06. The structure of myelin was well preserved in the adenosine-treated trauma group. However, the changes were irreversible in severely damaged areas. After acute spinal cord trauma, intravenous adenosine infusion of 100 micrograms/kg per minute could attenuate progression to secondary injury, but adenosine alone was not effective yet.