The roles of PKA in the remifentanil-induced hyperalgesia of rats undergoing abdominal incision hernia repair

Abstract

Objective The objective of this research was to investigate that proteinkinase A (PKA) may contribute to remifentanil-induced hyperalgesia (RIH) as the downstream of ephrinB/EphB signaling. Methods Aged male SD rats were made into abdominal wall hernia model. A week later, they were abdominal hernia repaired under remifentanil compound sevoflurane anesthesia. We characterized the remifentanil-induced pain behaviours by evaluating thermal hyperalgesia and mechanical allodynia in a rat hind paw. Protein expression of PKA in spinal cord was assayed by western blotting. Results Continuing infusion of remifentanil produced a thermal hyperalgesia and mechanical allodynia, which was accompanied with increased expression of spinal PKA protein, what appeared above was inhibited by pretreatment with EphB2-Fc, an antagonist of ephrinB/EphB.H89, inhibitors of PKA, suppressed pain behaviours induced by remifentanil infusion and reversed the increased pain behaviours induced by intrathecal injection of ephrinB2-Fc, an agonist of ephrinB/EphB. Conclusions Our findings confirmed that PKA is involved in remifentanil-induced hyperalgesia related to ephrinB/EphB signaling. EphrinB/ EphB signaling might be the upstream of PKA. This study provides fundamental theory for novel intervention targets for treatment of remifentanil-induedhyperalgesia. Key words: Abdominal incisional hernia; Remifentanil; Hyperalgesia