BACKGROUND: Although upregulation of cyclooxygenase (COX)-2 in spinal cord after peripheral inflammation has been well documented, the effect of surgery on spinal COX-2 has not been examined in detail. The present study uses a bilateral foot incision in rats to examine the magnitude and duration of surgically induced changes in spinal COX-2 protein. METHODS: A longitudinal incision was made in both plantar hind paws of isoflurane-anesthetized rats. Spinal cords were removed at various postoperative times (1-48 h), and spinal COX-2 protein levels were compared with the results of Western blot analysis. Ropivacaine-induced blockade of sciatic nerve function was used to determine the importance of afferent nerve activity on spinal COX-2 after incision. Dexamethasone and the COX-2-selective inhibitor L-745,337 were administered intrathecally to modulate spinal COX-2 after incision. RESULTS: COX-2 protein levels increased in the lumbar spinal cord at 3 (1.32-fold) and 6 (1.26-fold) h after bilateral foot incision. At later times, lumbar COX-2 levels were no different than in control animals not undergoing surgery. Cervical COX-2 protein levels remained unchanged. Sciatic nerve blockade with ropivacaine did not prevent the increase in lumbar spinal COX-2 protein levels after incision. Intrathecal dexamethasone decreased lumbar spinal COX-2 levels after incision, and an intrathecal COX-2-selective inhibitor did not reduce the COX-2 upregulation. CONCLUSIONS: After bilateral foot incision in rats, lumbar spinal COX-2 protein levels increase, although the magnitude and duration are less than reported in models of peripheral inflammation. This COX-2 upregulation does not seem to be mediated by afferent nerve activity.
BACKGROUND: Although upregulation of cyclooxygenase (COX)-2 in spinal cord after peripheral inflammation has been well documented, the effect of surgery on spinal COX-2 has not been examined in detail. The present study uses a bilateral foot incision in rats to examine the magnitude and duration of surgically induced changes in spinal COX-2 protein. METHODS: A longitudinal incision was made in both plantar hind paws of isoflurane-anesthetized rats. Spinal cords were removed at various postoperative times (1-48 h), and spinal COX-2 protein levels were compared with the results of Western blot analysis. Ropivacaine-induced blockade of sciatic nerve function was used to determine the importance of afferent nerve activity on spinal COX-2 after incision. Dexamethasone and the COX-2-selective inhibitor L-745,337 were administered intrathecally to modulate spinal COX-2 after incision. RESULTS:COX-2 protein levels increased in the lumbar spinal cord at 3 (1.32-fold) and 6 (1.26-fold) h after bilateral foot incision. At later times, lumbar COX-2 levels were no different than in control animals not undergoing surgery. Cervical COX-2 protein levels remained unchanged. Sciatic nerve blockade with ropivacaine did not prevent the increase in lumbar spinal COX-2 protein levels after incision. Intrathecal dexamethasone decreased lumbar spinal COX-2 levels after incision, and an intrathecal COX-2-selective inhibitor did not reduce the COX-2 upregulation. CONCLUSIONS: After bilateral foot incision in rats, lumbar spinal COX-2 protein levels increase, although the magnitude and duration are less than reported in models of peripheral inflammation. This COX-2 upregulation does not seem to be mediated by afferent nerve activity.