Effect of pre-emptive intrathecal administration of L-NAME on CGRP expression in spinal dorsal horn in a rat model of neuropathic pain / 中华麻醉学杂志

ABSTRACT

Objective To investigate the effect of pre-emptive intrathecal (IT) administration of L-NAME, a non-selective nitric oxide synthase (NOS) inhibitor on calcitonin gene-related peptide (CGRP) expression in the dorsal horn of spinal cord in a rat model of neuropathic pain. Methods Ninety-six female adult SD rats weighing 220-310 g were randomly divided into four groups with 24 animals in each group group A received IT 0.9% NaCl 15 min before sham operation; group B received IT 0.9% NaCl 15 min before right sciatic nerve ligation; group C received IT L-NAME 250 mg in 10?l 15 min before sham operation and group D received IT L-NAME 250 ?g in 10 ?l15 min before sciatic nerve ligation. The animals were anesthetized with intraperitoneal pentobarbital 50 mg?kg-1. A PE-10 catheter was placed in subarachnoid space with the tip of the catheter reaching the lumbar enlargement region. The animals were allowed to recover for 3-4 days and only those waking normally were used in the study. Right sciatic nerve was exposed and four loose ligatures were placed on the sciatic nerve according to the method described by Bennet. In sham operation the sciatic nerve was exposed but not ligated. The animals were sacrificed on the 1 st, 4 th, 7 th and 14 th day after operation. The lumbar segment of spinal cord was immediately removed. The CGRP expression in the ligated-side dorsal horn was assessed with immuno-histochemistry technique. Results In group B and D CGRP expression in the ligated side dorsal horn was significantly increased on the 4th, 7th and 14th day after operation as compared with that in group A. There was no significant difference in the CGRP expression in the ligated side dorsal horn between group A and C as well as between B and D. Conclusion Pre-emptive IT administration of L-NAME cannot inhibit the increase in CGRP expression in dorsal horn induced by peripheral nerve injury, suggesting that the neuropathic pain mediated by NO is not related to the release of calcitonin gene-related peptide.