Systemic lidocaine inhibits remifentanil-induced hyperalgesia via the inhibition of cPKCgamma membrane translocation in spinal dorsal horn of rats.

Remifentanil is being used increasingly as one component of total intravenous anesthesia. Severe postoperative pain has occasionally been reported with discontinuation of remifentanil. This study was designed to determine the involvement of conventional protein kinase Cgamma (cPKCgamma) in the inhibitory action of lidocaine on remifentanil-induced hyperalgesia of rats after propofol-remifentanil-based anesthesia. Male Sprague-Dawley rats were allocated into the following groups randomly: propofol only (P), propofol+remifentanil (R), propofol+remifentanil+lidocaine (RL), and propofol+lidocaine (L). Cumulative pain score and withdrawal response to mechanical stimulation, immunoblotting, and immunofluorescence were applied to observe remifentanil-induced hyperalgesia and cPKCgamma membrane translocation. We found that the cumulative pain score of group R increased significantly at 30, 120, and 300 minutes postanesthesia (P<0.05). After plantar incision, the withdrawal threshold on both the contralateral and the ipsilaeral side at 30, 120, and 300 minutes postanesthesia in group R was significantly lower than in groups P, RL, and L (P<0.05). Both immunoblotting and immunofluorescence showed that cPKCgamma membrane translocation increased in dorsal horn neurons of propofol-remifentanil-based anesthetized rats, which could be inhibited by systemic lidocaine. These results suggested that increased cPKCgamma membrane translocation was involved in remifentanil-induced hyperalgesia, which was inhibited by systemic lidocaine and may contribute to reduced postoperative pain in rats after propofol-remifentanil-based anesthesia.