ABSTRACT
Research conducted over the past 10 years has demonstrated that opiates can produce antinociception by peripheral as well as central mechanisms. Antinociception resulting from stimulation of peripheral opiate receptors has been reported in situations where chemical, thermal, or mechanical insult has resulted in hyperalgesia. Preclinical studies in rodents and clinical studies in humans have shown that potent antinociception results from injection of opiates directly into inflamed tissue at doses that are systemically inactive (1,2). Local actions of opiates are mediated through the µ, δ, and κ receptors (3-5), are stereoselective (3,4), reversible with antagonist treatment (4,5), and exhibit greater potency and efficacy compared with local (6) or systemic (7) administration of nonsteroidal anti-inflammatory agents (NSAIDs).
