The Experts below are selected from a list of 96 Experts worldwide ranked by ideXlab platform
Jack Bergman - One of the best experts on this subject based on the ideXlab platform.
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corrigendum to naloxonazine antagonism of Levorphanol induced antinociception and respiratory depression in rhesus monkeys eur j pharmacol 298 1996 31 36
European Journal of Pharmacology, 1996Co-Authors: Michael B Gatch, Anthony Liguori, Stevens S Negus, N K Mello, Jack BergmanAbstract:Abstract The μ-opioid receptor antagonist effects of naloxonazine on Levorphanol-induced thermal antinociception and respiratory depression were examined in rhesus monkeys. Levorphanol (0.032–3.2 mg/kg) produced dose-dependent increases in tail-withdrawal latencies from 50°C water in a warm-water tail-withdrawal assay and dose-dependent decreases in ventilation in both air and 5% CO 2 mixed in air. Naloxonazine (0.1–3.0 mg/kg) antagonized both the antinociceptive and ventilatory effects of Levorphanol to a similar degree, and the antagonist effects of naloxonazine were greater after 1 h than after 24 h. Under all conditions, the antagonist effects of naloxonazine were fully surmountable. Schild analysis of the antagonist effects of naloxonazine after 1 h pretreatment in the antinociception assay yielded a pA 2 value of 7.6 and a slope of −0.50; by comparison, quadazocine yielded a pA 2 value of 7.5 and a slope of −1.05. These results suggest that naloxonazine acts as a potent and fully reversible μ-opioid receptor antagonist with a moderately long duration of action in rhesus monkeys. In addition, these results suggest that the antinociceptive and ventilatory effects of μ-opioid receptor agonists in rhesus monkeys are mediated by pharmacologically similar popolations of μ-opioid receptors.
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Corrigendum to ‘Naloxonazine antagonism of Levorphanol-induced antinociception and respiratory depression in rhesus monkeys’ [Eur. J. Pharmacol. 298 (1996) 31–36]
European Journal of Pharmacology, 1996Co-Authors: Michael B Gatch, Anthony Liguori, Stevens S Negus, N K Mello, Jack BergmanAbstract:Abstract The μ-opioid receptor antagonist effects of naloxonazine on Levorphanol-induced thermal antinociception and respiratory depression were examined in rhesus monkeys. Levorphanol (0.032–3.2 mg/kg) produced dose-dependent increases in tail-withdrawal latencies from 50°C water in a warm-water tail-withdrawal assay and dose-dependent decreases in ventilation in both air and 5% CO 2 mixed in air. Naloxonazine (0.1–3.0 mg/kg) antagonized both the antinociceptive and ventilatory effects of Levorphanol to a similar degree, and the antagonist effects of naloxonazine were greater after 1 h than after 24 h. Under all conditions, the antagonist effects of naloxonazine were fully surmountable. Schild analysis of the antagonist effects of naloxonazine after 1 h pretreatment in the antinociception assay yielded a pA 2 value of 7.6 and a slope of −0.50; by comparison, quadazocine yielded a pA 2 value of 7.5 and a slope of −1.05. These results suggest that naloxonazine acts as a potent and fully reversible μ-opioid receptor antagonist with a moderately long duration of action in rhesus monkeys. In addition, these results suggest that the antinociceptive and ventilatory effects of μ-opioid receptor agonists in rhesus monkeys are mediated by pharmacologically similar popolations of μ-opioid receptors.
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Respiratory effects of opioid full and partial agonists in rhesus monkeys.
Journal of Pharmacology and Experimental Therapeutics, 1996Co-Authors: Anthony Liguori, W H Morse, Jack BergmanAbstract:Respiratory and behavioral effects of the mu selective opioids Levorphanol (0.01-3.0 mg/kg), methadone (0.03-5.6 mg/kg) and codeine (0.3-30.0 mg/kg) and the mixed-action opioids buprenorphine (0.003-10.0 mg/kg), butorphanol (0.003-0.3 mg/ kg) and nalbuphine (0.03-30.0 mg/kg) were studied in rhesus monkeys. In respiratory experiments, awake, seated monkeys wore plastic masks through which they breathed air or differing concentrations of CO2 mixed in air. Exposure to CO2 in air stimulated ventilation in a concentration-dependent manner. All opioids produced dose-dependent decreases in ventilation that were more pronounced as the concentration of CO2 increased. The highest doses of Levorphanol, methadone, and butorphanol reduced the ventilatory stimulant effects of 5% CO2 in air by 85 to 90%, whereas the highest doses of nalbuphine, buprenorphine and codeine reduced the effects of 5% CO2 in air by only 50 to 75%. After presession butorphanol (0.01-0.1 mg/kg) or nalbuphine (1.0-3.0 mg/kg), Levorphanol further reduced the ventilatory stimulant effects of 5% CO2 mixed in air, with some evidence of dose-effect flattening. However, pretreatment with buprenorphine (1.0-10.0 mg/kg) and the highest dose of nalbuphine (10.0 mg/kg) attenuated the effects of 10.0 mg/kg Levorphanol, indicative of antagonism. In behavioral experiments, all drugs produced dose-related decreases in responding under a 30-response fixed-ratio schedule. The highest doses of Levorphanol, methadone, codeine, and butorphanol nearly abolished responding in all subjects, whereas buprenorphine and nalbuphine most often reduced response rates by no more than 50%. Except for codeine, rank orders of potency were the same in behavioral and respiratory experiments. The lesser effects of nalbuphine and buprenorphine on ventilation, in conjunction with their Levorphanol-antagonist effects, suggest their limited mu agonist efficacy at sites mediating the respiratory-depressant effects of opioids.
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naloxonazine antagonism of Levorphanol induced antinociception and respiratory depression in rhesus monkeys
European Journal of Pharmacology, 1996Co-Authors: Michael B Gatch, Stevens S Negus, N K Mello, Tony Liguori, Jack BergmanAbstract:Abstract The μ-opioid receptor antagonist effects of naloxonazine on Levorphanol-induced thermal antinociception and respiratory depression were examined in rhesus monkeys. Levorphanol (0.032–3.2 mg/kg) produced dose-dependent increases in tail-withdrawal latencies from 50°C water in a warm-water tail-withdrawal assay and dose-dependent decreases in ventilation in both air and 5% CO 2 mixed in air. Naloxonazine (0.1–3.0 mg/kg) antagonized both the antinociceptive and ventilatory effects of Levorphanol to a similar degree, and the antagonist effects of naloxonazine were greater after 1 h than after 24 h. Under all conditions, the antagonist effects of naloxonazine were fully surmountable. Schild analysis of the antagonist effects of naloxonazine after 1 h pretreatment in the antinociception assay yielded a pA 2 value of 7.6 and a slope of −0.50; by comparison, quadazocine yielded a pA 2 value of 7.5 and a slope of −1.05. These results suggest that naloxonazine acts as a potent and fully reversible μ-opioid receptor antagonist with a moderately long duration of action in rhesus monkeys. In addition, these results suggest that the antinociceptive and ventilatory effects of μ-opioid receptor agonists in rhesus monkeys are mediated by pharmacologically similar populations of μ opioid receptors.
Michael B Gatch - One of the best experts on this subject based on the ideXlab platform.
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Corrigendum to ‘Naloxonazine antagonism of Levorphanol-induced antinociception and respiratory depression in rhesus monkeys’ [Eur. J. Pharmacol. 298 (1996) 31–36]
European Journal of Pharmacology, 1996Co-Authors: Michael B Gatch, Anthony Liguori, Stevens S Negus, N K Mello, Jack BergmanAbstract:Abstract The μ-opioid receptor antagonist effects of naloxonazine on Levorphanol-induced thermal antinociception and respiratory depression were examined in rhesus monkeys. Levorphanol (0.032–3.2 mg/kg) produced dose-dependent increases in tail-withdrawal latencies from 50°C water in a warm-water tail-withdrawal assay and dose-dependent decreases in ventilation in both air and 5% CO 2 mixed in air. Naloxonazine (0.1–3.0 mg/kg) antagonized both the antinociceptive and ventilatory effects of Levorphanol to a similar degree, and the antagonist effects of naloxonazine were greater after 1 h than after 24 h. Under all conditions, the antagonist effects of naloxonazine were fully surmountable. Schild analysis of the antagonist effects of naloxonazine after 1 h pretreatment in the antinociception assay yielded a pA 2 value of 7.6 and a slope of −0.50; by comparison, quadazocine yielded a pA 2 value of 7.5 and a slope of −1.05. These results suggest that naloxonazine acts as a potent and fully reversible μ-opioid receptor antagonist with a moderately long duration of action in rhesus monkeys. In addition, these results suggest that the antinociceptive and ventilatory effects of μ-opioid receptor agonists in rhesus monkeys are mediated by pharmacologically similar popolations of μ-opioid receptors.
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corrigendum to naloxonazine antagonism of Levorphanol induced antinociception and respiratory depression in rhesus monkeys eur j pharmacol 298 1996 31 36
European Journal of Pharmacology, 1996Co-Authors: Michael B Gatch, Anthony Liguori, Stevens S Negus, N K Mello, Jack BergmanAbstract:Abstract The μ-opioid receptor antagonist effects of naloxonazine on Levorphanol-induced thermal antinociception and respiratory depression were examined in rhesus monkeys. Levorphanol (0.032–3.2 mg/kg) produced dose-dependent increases in tail-withdrawal latencies from 50°C water in a warm-water tail-withdrawal assay and dose-dependent decreases in ventilation in both air and 5% CO 2 mixed in air. Naloxonazine (0.1–3.0 mg/kg) antagonized both the antinociceptive and ventilatory effects of Levorphanol to a similar degree, and the antagonist effects of naloxonazine were greater after 1 h than after 24 h. Under all conditions, the antagonist effects of naloxonazine were fully surmountable. Schild analysis of the antagonist effects of naloxonazine after 1 h pretreatment in the antinociception assay yielded a pA 2 value of 7.6 and a slope of −0.50; by comparison, quadazocine yielded a pA 2 value of 7.5 and a slope of −1.05. These results suggest that naloxonazine acts as a potent and fully reversible μ-opioid receptor antagonist with a moderately long duration of action in rhesus monkeys. In addition, these results suggest that the antinociceptive and ventilatory effects of μ-opioid receptor agonists in rhesus monkeys are mediated by pharmacologically similar popolations of μ-opioid receptors.
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naloxonazine antagonism of Levorphanol induced antinociception and respiratory depression in rhesus monkeys
European Journal of Pharmacology, 1996Co-Authors: Michael B Gatch, Stevens S Negus, N K Mello, Tony Liguori, Jack BergmanAbstract:Abstract The μ-opioid receptor antagonist effects of naloxonazine on Levorphanol-induced thermal antinociception and respiratory depression were examined in rhesus monkeys. Levorphanol (0.032–3.2 mg/kg) produced dose-dependent increases in tail-withdrawal latencies from 50°C water in a warm-water tail-withdrawal assay and dose-dependent decreases in ventilation in both air and 5% CO 2 mixed in air. Naloxonazine (0.1–3.0 mg/kg) antagonized both the antinociceptive and ventilatory effects of Levorphanol to a similar degree, and the antagonist effects of naloxonazine were greater after 1 h than after 24 h. Under all conditions, the antagonist effects of naloxonazine were fully surmountable. Schild analysis of the antagonist effects of naloxonazine after 1 h pretreatment in the antinociception assay yielded a pA 2 value of 7.6 and a slope of −0.50; by comparison, quadazocine yielded a pA 2 value of 7.5 and a slope of −1.05. These results suggest that naloxonazine acts as a potent and fully reversible μ-opioid receptor antagonist with a moderately long duration of action in rhesus monkeys. In addition, these results suggest that the antinociceptive and ventilatory effects of μ-opioid receptor agonists in rhesus monkeys are mediated by pharmacologically similar populations of μ opioid receptors.
Dirk K F Meijer - One of the best experts on this subject based on the ideXlab platform.
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identification with liquid chromatography ionspray mass spectrometry of the metabolites of the enantiomers n methyl dextrorphan and n methyl Levorphanol after rat liver perfusion
Journal of Mass Spectrometry, 1993Co-Authors: A B L Lanting, A P Bruins, B F H Drenth, K De Jonge, K Ensing, R A De Zeeuw, Dirk K F MeijerAbstract:To gather more information on stereochemical factors in the hepatic disposition of organic cations, mass spectrometry coupled to liquid chromatography was used to determine the identity of the metabolites excreted in bile after isolated rat liver perfusions with the quaternary ammonium derivatives of the enantiomeric drugs dextrorphan and Levorphanol. Ionspray mass spectrometry was chosen for its soft ionization and absence of thermal degradation of labile compounds. The drugs were labelled with a stable (H-2) isotope and mixed with unlabelled drugs to create an artificial isotope pattern in the mass spectrum and facilitate the recognition of unknown metabolites. In mass spectra that were recorded under normal conditions, fragmentation was absent and metabolites of N-methyl dextrorphan and N-methyl Levorphanol were visible as parent-ion 'doublets'. Collision-induced fragmentation studies were performed to support the identification of the metabolites. For N-methyl dextrorphan the glucuronide, the glutathione conjugate and the glucuronide of the N-demethylated metabolite were found in bile. For N-methyl Levorphanol the glucuronide, the glutathione conjugate, the sulphate conjugate and the glucuronide of a hydroxylated N-methyl Levorphanol were excreted in bile. Thus a remarkable stereoselectivity occurs in the metabolism of these quaternary ammonium compounds in the rat liver.
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Identification with liquid chromatography–ionspray mass spectrometry of the metabolites of the enantiomers N‐methyl dextrorphan and N‐methyl Levorphanol after rat liver perfusion
Journal of Mass Spectrometry, 1993Co-Authors: A B L Lanting, A P Bruins, B F H Drenth, K De Jonge, K Ensing, R A De Zeeuw, Dirk K F MeijerAbstract:To gather more information on stereochemical factors in the hepatic disposition of organic cations, mass spectrometry coupled to liquid chromatography was used to determine the identity of the metabolites excreted in bile after isolated rat liver perfusions with the quaternary ammonium derivatives of the enantiomeric drugs dextrorphan and Levorphanol. Ionspray mass spectrometry was chosen for its soft ionization and absence of thermal degradation of labile compounds. The drugs were labelled with a stable (H-2) isotope and mixed with unlabelled drugs to create an artificial isotope pattern in the mass spectrum and facilitate the recognition of unknown metabolites. In mass spectra that were recorded under normal conditions, fragmentation was absent and metabolites of N-methyl dextrorphan and N-methyl Levorphanol were visible as parent-ion 'doublets'. Collision-induced fragmentation studies were performed to support the identification of the metabolites. For N-methyl dextrorphan the glucuronide, the glutathione conjugate and the glucuronide of the N-demethylated metabolite were found in bile. For N-methyl Levorphanol the glucuronide, the glutathione conjugate, the sulphate conjugate and the glucuronide of a hydroxylated N-methyl Levorphanol were excreted in bile. Thus a remarkable stereoselectivity occurs in the metabolism of these quaternary ammonium compounds in the rat liver.
Stevens S Negus - One of the best experts on this subject based on the ideXlab platform.
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Corrigendum to ‘Naloxonazine antagonism of Levorphanol-induced antinociception and respiratory depression in rhesus monkeys’ [Eur. J. Pharmacol. 298 (1996) 31–36]
European Journal of Pharmacology, 1996Co-Authors: Michael B Gatch, Anthony Liguori, Stevens S Negus, N K Mello, Jack BergmanAbstract:Abstract The μ-opioid receptor antagonist effects of naloxonazine on Levorphanol-induced thermal antinociception and respiratory depression were examined in rhesus monkeys. Levorphanol (0.032–3.2 mg/kg) produced dose-dependent increases in tail-withdrawal latencies from 50°C water in a warm-water tail-withdrawal assay and dose-dependent decreases in ventilation in both air and 5% CO 2 mixed in air. Naloxonazine (0.1–3.0 mg/kg) antagonized both the antinociceptive and ventilatory effects of Levorphanol to a similar degree, and the antagonist effects of naloxonazine were greater after 1 h than after 24 h. Under all conditions, the antagonist effects of naloxonazine were fully surmountable. Schild analysis of the antagonist effects of naloxonazine after 1 h pretreatment in the antinociception assay yielded a pA 2 value of 7.6 and a slope of −0.50; by comparison, quadazocine yielded a pA 2 value of 7.5 and a slope of −1.05. These results suggest that naloxonazine acts as a potent and fully reversible μ-opioid receptor antagonist with a moderately long duration of action in rhesus monkeys. In addition, these results suggest that the antinociceptive and ventilatory effects of μ-opioid receptor agonists in rhesus monkeys are mediated by pharmacologically similar popolations of μ-opioid receptors.
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corrigendum to naloxonazine antagonism of Levorphanol induced antinociception and respiratory depression in rhesus monkeys eur j pharmacol 298 1996 31 36
European Journal of Pharmacology, 1996Co-Authors: Michael B Gatch, Anthony Liguori, Stevens S Negus, N K Mello, Jack BergmanAbstract:Abstract The μ-opioid receptor antagonist effects of naloxonazine on Levorphanol-induced thermal antinociception and respiratory depression were examined in rhesus monkeys. Levorphanol (0.032–3.2 mg/kg) produced dose-dependent increases in tail-withdrawal latencies from 50°C water in a warm-water tail-withdrawal assay and dose-dependent decreases in ventilation in both air and 5% CO 2 mixed in air. Naloxonazine (0.1–3.0 mg/kg) antagonized both the antinociceptive and ventilatory effects of Levorphanol to a similar degree, and the antagonist effects of naloxonazine were greater after 1 h than after 24 h. Under all conditions, the antagonist effects of naloxonazine were fully surmountable. Schild analysis of the antagonist effects of naloxonazine after 1 h pretreatment in the antinociception assay yielded a pA 2 value of 7.6 and a slope of −0.50; by comparison, quadazocine yielded a pA 2 value of 7.5 and a slope of −1.05. These results suggest that naloxonazine acts as a potent and fully reversible μ-opioid receptor antagonist with a moderately long duration of action in rhesus monkeys. In addition, these results suggest that the antinociceptive and ventilatory effects of μ-opioid receptor agonists in rhesus monkeys are mediated by pharmacologically similar popolations of μ-opioid receptors.
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naloxonazine antagonism of Levorphanol induced antinociception and respiratory depression in rhesus monkeys
European Journal of Pharmacology, 1996Co-Authors: Michael B Gatch, Stevens S Negus, N K Mello, Tony Liguori, Jack BergmanAbstract:Abstract The μ-opioid receptor antagonist effects of naloxonazine on Levorphanol-induced thermal antinociception and respiratory depression were examined in rhesus monkeys. Levorphanol (0.032–3.2 mg/kg) produced dose-dependent increases in tail-withdrawal latencies from 50°C water in a warm-water tail-withdrawal assay and dose-dependent decreases in ventilation in both air and 5% CO 2 mixed in air. Naloxonazine (0.1–3.0 mg/kg) antagonized both the antinociceptive and ventilatory effects of Levorphanol to a similar degree, and the antagonist effects of naloxonazine were greater after 1 h than after 24 h. Under all conditions, the antagonist effects of naloxonazine were fully surmountable. Schild analysis of the antagonist effects of naloxonazine after 1 h pretreatment in the antinociception assay yielded a pA 2 value of 7.6 and a slope of −0.50; by comparison, quadazocine yielded a pA 2 value of 7.5 and a slope of −1.05. These results suggest that naloxonazine acts as a potent and fully reversible μ-opioid receptor antagonist with a moderately long duration of action in rhesus monkeys. In addition, these results suggest that the antinociceptive and ventilatory effects of μ-opioid receptor agonists in rhesus monkeys are mediated by pharmacologically similar populations of μ opioid receptors.
N K Mello - One of the best experts on this subject based on the ideXlab platform.
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Corrigendum to ‘Naloxonazine antagonism of Levorphanol-induced antinociception and respiratory depression in rhesus monkeys’ [Eur. J. Pharmacol. 298 (1996) 31–36]
European Journal of Pharmacology, 1996Co-Authors: Michael B Gatch, Anthony Liguori, Stevens S Negus, N K Mello, Jack BergmanAbstract:Abstract The μ-opioid receptor antagonist effects of naloxonazine on Levorphanol-induced thermal antinociception and respiratory depression were examined in rhesus monkeys. Levorphanol (0.032–3.2 mg/kg) produced dose-dependent increases in tail-withdrawal latencies from 50°C water in a warm-water tail-withdrawal assay and dose-dependent decreases in ventilation in both air and 5% CO 2 mixed in air. Naloxonazine (0.1–3.0 mg/kg) antagonized both the antinociceptive and ventilatory effects of Levorphanol to a similar degree, and the antagonist effects of naloxonazine were greater after 1 h than after 24 h. Under all conditions, the antagonist effects of naloxonazine were fully surmountable. Schild analysis of the antagonist effects of naloxonazine after 1 h pretreatment in the antinociception assay yielded a pA 2 value of 7.6 and a slope of −0.50; by comparison, quadazocine yielded a pA 2 value of 7.5 and a slope of −1.05. These results suggest that naloxonazine acts as a potent and fully reversible μ-opioid receptor antagonist with a moderately long duration of action in rhesus monkeys. In addition, these results suggest that the antinociceptive and ventilatory effects of μ-opioid receptor agonists in rhesus monkeys are mediated by pharmacologically similar popolations of μ-opioid receptors.
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corrigendum to naloxonazine antagonism of Levorphanol induced antinociception and respiratory depression in rhesus monkeys eur j pharmacol 298 1996 31 36
European Journal of Pharmacology, 1996Co-Authors: Michael B Gatch, Anthony Liguori, Stevens S Negus, N K Mello, Jack BergmanAbstract:Abstract The μ-opioid receptor antagonist effects of naloxonazine on Levorphanol-induced thermal antinociception and respiratory depression were examined in rhesus monkeys. Levorphanol (0.032–3.2 mg/kg) produced dose-dependent increases in tail-withdrawal latencies from 50°C water in a warm-water tail-withdrawal assay and dose-dependent decreases in ventilation in both air and 5% CO 2 mixed in air. Naloxonazine (0.1–3.0 mg/kg) antagonized both the antinociceptive and ventilatory effects of Levorphanol to a similar degree, and the antagonist effects of naloxonazine were greater after 1 h than after 24 h. Under all conditions, the antagonist effects of naloxonazine were fully surmountable. Schild analysis of the antagonist effects of naloxonazine after 1 h pretreatment in the antinociception assay yielded a pA 2 value of 7.6 and a slope of −0.50; by comparison, quadazocine yielded a pA 2 value of 7.5 and a slope of −1.05. These results suggest that naloxonazine acts as a potent and fully reversible μ-opioid receptor antagonist with a moderately long duration of action in rhesus monkeys. In addition, these results suggest that the antinociceptive and ventilatory effects of μ-opioid receptor agonists in rhesus monkeys are mediated by pharmacologically similar popolations of μ-opioid receptors.
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naloxonazine antagonism of Levorphanol induced antinociception and respiratory depression in rhesus monkeys
European Journal of Pharmacology, 1996Co-Authors: Michael B Gatch, Stevens S Negus, N K Mello, Tony Liguori, Jack BergmanAbstract:Abstract The μ-opioid receptor antagonist effects of naloxonazine on Levorphanol-induced thermal antinociception and respiratory depression were examined in rhesus monkeys. Levorphanol (0.032–3.2 mg/kg) produced dose-dependent increases in tail-withdrawal latencies from 50°C water in a warm-water tail-withdrawal assay and dose-dependent decreases in ventilation in both air and 5% CO 2 mixed in air. Naloxonazine (0.1–3.0 mg/kg) antagonized both the antinociceptive and ventilatory effects of Levorphanol to a similar degree, and the antagonist effects of naloxonazine were greater after 1 h than after 24 h. Under all conditions, the antagonist effects of naloxonazine were fully surmountable. Schild analysis of the antagonist effects of naloxonazine after 1 h pretreatment in the antinociception assay yielded a pA 2 value of 7.6 and a slope of −0.50; by comparison, quadazocine yielded a pA 2 value of 7.5 and a slope of −1.05. These results suggest that naloxonazine acts as a potent and fully reversible μ-opioid receptor antagonist with a moderately long duration of action in rhesus monkeys. In addition, these results suggest that the antinociceptive and ventilatory effects of μ-opioid receptor agonists in rhesus monkeys are mediated by pharmacologically similar populations of μ opioid receptors.