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 (cPKC gamma) in the inhibitory action of lidocaine oil 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 cPKC gamma 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 oil 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 cPKC gamma 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 cPKC gamma 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.