Hiperalgesia inducida por opioidesimplicación durante la anestesia inhalatoria en la rata

Abstract

Opioids are the drugs of choice in perioperative pain management and combined with anaesthetics provide the analgesic component of a balanced anaesthetic regimen. Increasing evidence suggest that opioids not only promote antinociceptive effects (analgesia), but can simultaneously activate pronociceptive effects leading to opioid-induced hyperalgesia. The aim of this study was to determine whether previous opioid administration leading to hyperalgesia may be associated with increased inhalant anaesthetic requirements. Several studies have been performed in rats anesthetized with sevoflurane aiming to determine 1) the dose-dependent and immediate MAC reduction produced by butorphanol, methadone, morphine, and tramadol, 2) the delayed increases on MAC produced by buprenorphine, methadone, morphine, remifentanil and tramadol, associated with lasting hyperalgesia 3) the remifentanil and 4) tramadol induced hyperalgesia and associated increases in the MAC and 5) whether these effects may be prevented by ketamine. All studied opioids reduced the MAC immediately but were followed by a latter increase in basal sevoflurane requirements lasting at least 21 days. This effect was associated with hyperalgesia when remifentanil and tramadol were used. Finally, the hyperalgesia and MAC increase produced by tramadol were prevented by ketamine.