Buprenorphine is a potent analgesic with μ-agonistic and κ-antagonistic opioid properties. In patients, buprenorphine is used for treatment of chronic pain using various administration modes, such as transdermal, sublingual or spinal administration. In humans, buprenorphine behaves as a typical μ-opioid agonist showing analgesia, respiratory depression and constriction of the pupils. Buprenorphine has high affinity for opioid receptors and slower receptor dissociation as compared to other opioids. After intravenous infusion, the duration of action is about 6 to 8 hours, with a speed of onset of effect of about 15 min. Using a human model, we assessed the effects of buprenorphine on analgesia and respiration to address the following questions:

(1) How do the analgesic and respiratory effects of buprenorphine compare at various buprenorphine concentrations?

(2) How do the respiratory effects of buprenorphine compare to the respiratory effects of the μ-agonistic fentanyl?

(3) Are we able to easily reverse the respiratory depressant effects using the μ-receptor antagonist naloxone?

Studies were performed in healthy young volunteers, free from underlying disease.

Our data indicate that buprenorphine is a potent analgesic with limited respiratory effect (due to the "ceiling" phenomenon) and displays favorable respiratory pharmacodynamics relative to other potent opioids such as fentanyl. The reversal of buprenorphine's effect is relatively easy when a continuous plasma concentration of naloxone is available.