Effect of naloxone on primary and secondary hyperalgesia induced by the human burn injury model

Background: Opioid antagonists may change the responses in models of experi mental hyperalgesia. This indicates a possible involvement of the endogenou s opioid system in these models. The aim of the present study was to evalua te whether activation of the endogenous opioid system could be demonstrated in the human burn injury model of cutaneous hyperalgesia, using an intrave nous challenge with the non-selective opioid antagonist naloxone. Methods: We studied 25 healthy male volunteers aged 20-31 yrs in a randomis ed, double-blind, triple crossover design. A 25 X 50 mm rectangular burn in jury was produced on the calf on 3 separate days, at least I week apart. Su bjects received an intravenous bolus dose of naloxone 0.4 mg, 10 mg or plac ebo 3 h after induction of the burn injury. Results: Primary and secondary hyperalgesia was induced by the burn injury. Naloxone did not affect any of the measured variables: heat pain detection threshold in non-injured or injured tissue, pain produced by short or prol onged noxious heat in non-injured or injured tissue, secondary hyperalgesia elicited by pin prick or stroke, or pain produced by short or prolonged no xious mechanical stimulation in non-injured tissue. No significant adverse effects of naloxone were encountered. Conclusions: Activation of an endogenous opioid response following inductio n of hyperalgesia in human volunteers by a burn injury could not be demonst rated with an intravenous naloxone challenge. These findings suggest that t he endogenous opioid response is not a confounding factor in this model.