This study was designed to analyze the effect of early indomethacin on the
lipid peroxidation after spinal cord injury in rats. The use of anti-inflam
matory drugs to affect delayed and secondary injury after trauma to the spi
nal cord has now become a matter of standard clinical practice. However, sp
inal cord injury remains an enormous clinical problem and research that may
lead to improved treatment is to be encouraged and commended. Three experi
mental groups consisting of 40 rats each were formed. Using microsurgical t
echnique, total laminectomy between T5 and T10 was performed. Spinal cord i
njury was achieved with an epidural aneurysm clip, and pharmacological trea
tment immediate after the injury was performed by injecting indomethacin in
traperitoneally (i.p.) at a dose of 3 mg/kg to indomethacin-treated group.
The three main groups were divided into subgroups of 8 rats each. It was pl
anned to stop the biochemical reactions at a different time in each of thes
e subgroups, by the application of liquid nitrogen to the spinal cord and p
aravertebral structures at the end of the 1st, 15th, 30th, 60th, and 90th m
inutes. All the spinal cords were removed and protected from further reacti
ons by immersing in the liquid nitrogen tank. The lipid peroxidation levels
were assessed by determining thiobarbituric acid reactive substances forma
tion. The results of the study showed that the administration of 3 mg/kg in
domethacin immediately after spinal cord injury induces lipid peroxidation
to a significant degree (p < 0.05 one-way ANOVA and Tukey HSD tests) when c
ompared to the saline-treated group. This result suggests that early posttr
aumatic indomethacin treatment may be harmful in spinal cord injury. Copyri
ght (C) 2000 S. Karger AG, Basel.