Magnesium sulphate attenuate remifentanil-induced postoperative hyperalgesia via regulating tyrosine phosphorylation of the NRB subunit of the NMDA receptor in the spinal cord.

Background: Remifentanil induced hyperalgesia (RIH) is characterized by stimulation evoked pain including allodynia and thermal hyperalgesia after remifentanil infusion. N-methyl-D-aspartate (NMDA) receptor was reported to be involved in the progress of RIH. We hypothesized that intrathecal MgSO could relieve hyperalgesia after remifentanil infusion via regulating phosphorylation of NMDA receptor NRB subunit activity in this study.

Methods: Thirty two rats were randomly allocated into control group, model of RIH group, RIH plus 100ug MgSO group, RIH plus 300ug MgSO group. Mechanical and thermal hyperalgesia were tested at -24 h, 2 h, 6 h, 24 h, 48 h after remifentanil infusion. Following sacrifice of rats after the last behavioral test, we performed the western blot to detect the expression of spinal phosphorylated NMDA receptor NRB subunit (pNRB) in the L-L segments.

Results: Intrathecal MgSO (100, 300 μg) dose-dependently reduced thermal and mechanical hyperalgesia from 2 h to 48 h after remifentanil infusion. Remifentanil infusion remarkably stimulated the expression of pNRB. Nevertheless, the increased amount of pNRB by RIH was dose-dependently suppressed by intrathecal infusion of MgSO in rats.

Conclusions: Remifentanil induced hyperalgesia/allodynia could be ameliorated by Mg-mediated blockade targeting the NRB subunit in NMDA receptors.