Cannabinoid modulation of opioid analgesia and subjective drug effects in healthy humans
Rationale Dozens of preclinical studies have reported cannabinoid agonist potentiation of the analgesic effects of μ-opioid agonists. Objectives The aim of this study was to determine if a cannabinoid agonist could potentiate opioid analgesia in humans using several laboratory pain models. Methods H...
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| Published in | Psychopharmacology Vol. 236; no. 11; pp. 3341 - 3352 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Berlin/Heidelberg
Springer Berlin Heidelberg
01.11.2019
Springer Springer Nature B.V |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0033-3158 1432-2072 1432-2072 |
| DOI | 10.1007/s00213-019-05293-1 |
Cover
| Abstract | Rationale
Dozens of preclinical studies have reported cannabinoid agonist potentiation of the analgesic effects of μ-opioid agonists.
Objectives
The aim of this study was to determine if a cannabinoid agonist could potentiate opioid analgesia in humans using several laboratory pain models.
Methods
Healthy participants (
n
= 10) with/out current drug use/pain conditions completed this within-subject, double-blind, placebo-controlled, randomized outpatient study. Nine 8-h sessions were completed during which dronabinol (0, 2.5, 5 mg, p.o.) was administered 1 h before oxycodone (0, 5, 10 mg, p.o.) for a total of 9 test conditions. Outcomes included sensory threshold and tolerance from four experimental pain models (cold pressor, pressure algometer, hot thermode, cold hyperalgesia), along with participant- and observer-rated, performance and physiological effects.
Results
Oxycodone produced miosis (
p
< 0.05) and analgesic responses (e.g., pressure algometer [
p
< 0.05]), while dronabinol did not (
p
> 0.05). Depending on the dose combination, dronabinol attenuated or did not alter oxycodone analgesia; for example, dronabinol (2.5 mg) decreased the analgesic effects of oxycodone (10 mg) on pressure tolerance. Conversely, dronabinol increased oxycodone subjective effects (e.g., drug liking) (
p
< 0.05); oxycodone (5 mg) ratings of “high” were potentiated by 5 mg dronabinol (
p
< 0.05; placebo = 1.1 [± 0.7]; 5 mg oxycodone = 4.7 [± 2.2]; 5 mg dronabinol = 9.9 [± 8.4]; 5 mg oxycodone + 5 mg dronabinol = 37.4 [± 11.3]).
Conclusions
This study indicates that dronabinol did not enhance the analgesic effects of oxycodone and increased abuse- and impairment-related subjective effects. These data suggest that dronabinol may not be an effective or appropriate opioid adjuvant; it could potentially increase opioid dose requirements, while increasing psychoactive opioid effects. |
|---|---|
| AbstractList | Dozens of preclinical studies have reported cannabinoid agonist potentiation of the analgesic effects of μ-opioid agonists.
The aim of this study was to determine if a cannabinoid agonist could potentiate opioid analgesia in humans using several laboratory pain models.
Healthy participants (n = 10) with/out current drug use/pain conditions completed this within-subject, double-blind, placebo-controlled, randomized outpatient study. Nine 8-h sessions were completed during which dronabinol (0, 2.5, 5 mg, p.o.) was administered 1 h before oxycodone (0, 5, 10 mg, p.o.) for a total of 9 test conditions. Outcomes included sensory threshold and tolerance from four experimental pain models (cold pressor, pressure algometer, hot thermode, cold hyperalgesia), along with participant- and observer-rated, performance and physiological effects.
Oxycodone produced miosis (p < 0.05) and analgesic responses (e.g., pressure algometer [p < 0.05]), while dronabinol did not (p > 0.05). Depending on the dose combination, dronabinol attenuated or did not alter oxycodone analgesia; for example, dronabinol (2.5 mg) decreased the analgesic effects of oxycodone (10 mg) on pressure tolerance. Conversely, dronabinol increased oxycodone subjective effects (e.g., drug liking) (p < 0.05); oxycodone (5 mg) ratings of "high" were potentiated by 5 mg dronabinol (p < 0.05; placebo = 1.1 [± 0.7]; 5 mg oxycodone = 4.7 [± 2.2]; 5 mg dronabinol = 9.9 [± 8.4]; 5 mg oxycodone + 5 mg dronabinol = 37.4 [± 11.3]).
This study indicates that dronabinol did not enhance the analgesic effects of oxycodone and increased abuse- and impairment-related subjective effects. These data suggest that dronabinol may not be an effective or appropriate opioid adjuvant; it could potentially increase opioid dose requirements, while increasing psychoactive opioid effects. Rationale Dozens of preclinical studies have reported cannabinoid agonist potentiation of the analgesic effects of μ-opioid agonists. Objectives The aim of this study was to determine if a cannabinoid agonist could potentiate opioid analgesia in humans using several laboratory pain models. Methods Healthy participants ( n = 10) with/out current drug use/pain conditions completed this within-subject, double-blind, placebo-controlled, randomized outpatient study. Nine 8-h sessions were completed during which dronabinol (0, 2.5, 5 mg, p.o.) was administered 1 h before oxycodone (0, 5, 10 mg, p.o.) for a total of 9 test conditions. Outcomes included sensory threshold and tolerance from four experimental pain models (cold pressor, pressure algometer, hot thermode, cold hyperalgesia), along with participant- and observer-rated, performance and physiological effects. Results Oxycodone produced miosis ( p < 0.05) and analgesic responses (e.g., pressure algometer [ p < 0.05]), while dronabinol did not ( p > 0.05). Depending on the dose combination, dronabinol attenuated or did not alter oxycodone analgesia; for example, dronabinol (2.5 mg) decreased the analgesic effects of oxycodone (10 mg) on pressure tolerance. Conversely, dronabinol increased oxycodone subjective effects (e.g., drug liking) ( p < 0.05); oxycodone (5 mg) ratings of “high” were potentiated by 5 mg dronabinol ( p < 0.05; placebo = 1.1 [± 0.7]; 5 mg oxycodone = 4.7 [± 2.2]; 5 mg dronabinol = 9.9 [± 8.4]; 5 mg oxycodone + 5 mg dronabinol = 37.4 [± 11.3]). Conclusions This study indicates that dronabinol did not enhance the analgesic effects of oxycodone and increased abuse- and impairment-related subjective effects. These data suggest that dronabinol may not be an effective or appropriate opioid adjuvant; it could potentially increase opioid dose requirements, while increasing psychoactive opioid effects. Rationale Dozens of preclinical studies have reported cannabinoid agonist potentiation of the analgesic effects of [mu]-opioid agonists. Objectives The aim of this study was to determine if a cannabinoid agonist could potentiate opioid analgesia in humans using several laboratory pain models. Methods Healthy participants (n = 10) with/out current drug use/pain conditions completed this within-subject, double-blind, placebo-controlled, randomized outpatient study. Nine 8-h sessions were completed during which dronabinol (0, 2.5, 5 mg, p.o.) was administered 1 h before oxycodone (0, 5, 10 mg, p.o.) for a total of 9 test conditions. Outcomes included sensory threshold and tolerance from four experimental pain models (cold pressor, pressure algometer, hot thermode, cold hyperalgesia), along with participant- and observer-rated, performance and physiological effects. Results Oxycodone produced miosis (p < 0.05) and analgesic responses (e.g., pressure algometer [p < 0.05]), while dronabinol did not (p > 0.05). Depending on the dose combination, dronabinol attenuated or did not alter oxycodone analgesia; for example, dronabinol (2.5 mg) decreased the analgesic effects of oxycodone (10 mg) on pressure tolerance. Conversely, dronabinol increased oxycodone subjective effects (e.g., drug liking) (p < 0.05); oxycodone (5 mg) ratings of "high" were potentiated by 5 mg dronabinol (p < 0.05; placebo = 1.1 [± 0.7]; 5 mg oxycodone = 4.7 [± 2.2]; 5 mg dronabinol = 9.9 [± 8.4]; 5 mg oxycodone + 5 mg dronabinol = 37.4 [± 11.3]). Conclusions This study indicates that dronabinol did not enhance the analgesic effects of oxycodone and increased abuse- and impairment-related subjective effects. These data suggest that dronabinol may not be an effective or appropriate opioid adjuvant; it could potentially increase opioid dose requirements, while increasing psychoactive opioid effects. Dozens of preclinical studies have reported cannabinoid agonist potentiation of the analgesic effects of [mu]-opioid agonists. The aim of this study was to determine if a cannabinoid agonist could potentiate opioid analgesia in humans using several laboratory pain models. Healthy participants (n = 10) with/out current drug use/pain conditions completed this within-subject, double-blind, placebo-controlled, randomized outpatient study. Nine 8-h sessions were completed during which dronabinol (0, 2.5, 5 mg, p.o.) was administered 1 h before oxycodone (0, 5, 10 mg, p.o.) for a total of 9 test conditions. Outcomes included sensory threshold and tolerance from four experimental pain models (cold pressor, pressure algometer, hot thermode, cold hyperalgesia), along with participant- and observer-rated, performance and physiological effects. Oxycodone produced miosis (p < 0.05) and analgesic responses (e.g., pressure algometer [p < 0.05]), while dronabinol did not (p > 0.05). Depending on the dose combination, dronabinol attenuated or did not alter oxycodone analgesia; for example, dronabinol (2.5 mg) decreased the analgesic effects of oxycodone (10 mg) on pressure tolerance. Conversely, dronabinol increased oxycodone subjective effects (e.g., drug liking) (p < 0.05); oxycodone (5 mg) ratings of "high" were potentiated by 5 mg dronabinol (p < 0.05; placebo = 1.1 [± 0.7]; 5 mg oxycodone = 4.7 [± 2.2]; 5 mg dronabinol = 9.9 [± 8.4]; 5 mg oxycodone + 5 mg dronabinol = 37.4 [± 11.3]). This study indicates that dronabinol did not enhance the analgesic effects of oxycodone and increased abuse- and impairment-related subjective effects. These data suggest that dronabinol may not be an effective or appropriate opioid adjuvant; it could potentially increase opioid dose requirements, while increasing psychoactive opioid effects. RationaleDozens of preclinical studies have reported cannabinoid agonist potentiation of the analgesic effects of μ-opioid agonists.ObjectivesThe aim of this study was to determine if a cannabinoid agonist could potentiate opioid analgesia in humans using several laboratory pain models.MethodsHealthy participants (n = 10) with/out current drug use/pain conditions completed this within-subject, double-blind, placebo-controlled, randomized outpatient study. Nine 8-h sessions were completed during which dronabinol (0, 2.5, 5 mg, p.o.) was administered 1 h before oxycodone (0, 5, 10 mg, p.o.) for a total of 9 test conditions. Outcomes included sensory threshold and tolerance from four experimental pain models (cold pressor, pressure algometer, hot thermode, cold hyperalgesia), along with participant- and observer-rated, performance and physiological effects.ResultsOxycodone produced miosis (p < 0.05) and analgesic responses (e.g., pressure algometer [p < 0.05]), while dronabinol did not (p > 0.05). Depending on the dose combination, dronabinol attenuated or did not alter oxycodone analgesia; for example, dronabinol (2.5 mg) decreased the analgesic effects of oxycodone (10 mg) on pressure tolerance. Conversely, dronabinol increased oxycodone subjective effects (e.g., drug liking) (p < 0.05); oxycodone (5 mg) ratings of “high” were potentiated by 5 mg dronabinol (p < 0.05; placebo = 1.1 [± 0.7]; 5 mg oxycodone = 4.7 [± 2.2]; 5 mg dronabinol = 9.9 [± 8.4]; 5 mg oxycodone + 5 mg dronabinol = 37.4 [± 11.3]).ConclusionsThis study indicates that dronabinol did not enhance the analgesic effects of oxycodone and increased abuse- and impairment-related subjective effects. These data suggest that dronabinol may not be an effective or appropriate opioid adjuvant; it could potentially increase opioid dose requirements, while increasing psychoactive opioid effects. Dozens of preclinical studies have reported cannabinoid agonist potentiation of the analgesic effects of μ-opioid agonists.RATIONALEDozens of preclinical studies have reported cannabinoid agonist potentiation of the analgesic effects of μ-opioid agonists.The aim of this study was to determine if a cannabinoid agonist could potentiate opioid analgesia in humans using several laboratory pain models.OBJECTIVESThe aim of this study was to determine if a cannabinoid agonist could potentiate opioid analgesia in humans using several laboratory pain models.Healthy participants (n = 10) with/out current drug use/pain conditions completed this within-subject, double-blind, placebo-controlled, randomized outpatient study. Nine 8-h sessions were completed during which dronabinol (0, 2.5, 5 mg, p.o.) was administered 1 h before oxycodone (0, 5, 10 mg, p.o.) for a total of 9 test conditions. Outcomes included sensory threshold and tolerance from four experimental pain models (cold pressor, pressure algometer, hot thermode, cold hyperalgesia), along with participant- and observer-rated, performance and physiological effects.METHODSHealthy participants (n = 10) with/out current drug use/pain conditions completed this within-subject, double-blind, placebo-controlled, randomized outpatient study. Nine 8-h sessions were completed during which dronabinol (0, 2.5, 5 mg, p.o.) was administered 1 h before oxycodone (0, 5, 10 mg, p.o.) for a total of 9 test conditions. Outcomes included sensory threshold and tolerance from four experimental pain models (cold pressor, pressure algometer, hot thermode, cold hyperalgesia), along with participant- and observer-rated, performance and physiological effects.Oxycodone produced miosis (p < 0.05) and analgesic responses (e.g., pressure algometer [p < 0.05]), while dronabinol did not (p > 0.05). Depending on the dose combination, dronabinol attenuated or did not alter oxycodone analgesia; for example, dronabinol (2.5 mg) decreased the analgesic effects of oxycodone (10 mg) on pressure tolerance. Conversely, dronabinol increased oxycodone subjective effects (e.g., drug liking) (p < 0.05); oxycodone (5 mg) ratings of "high" were potentiated by 5 mg dronabinol (p < 0.05; placebo = 1.1 [± 0.7]; 5 mg oxycodone = 4.7 [± 2.2]; 5 mg dronabinol = 9.9 [± 8.4]; 5 mg oxycodone + 5 mg dronabinol = 37.4 [± 11.3]).RESULTSOxycodone produced miosis (p < 0.05) and analgesic responses (e.g., pressure algometer [p < 0.05]), while dronabinol did not (p > 0.05). Depending on the dose combination, dronabinol attenuated or did not alter oxycodone analgesia; for example, dronabinol (2.5 mg) decreased the analgesic effects of oxycodone (10 mg) on pressure tolerance. Conversely, dronabinol increased oxycodone subjective effects (e.g., drug liking) (p < 0.05); oxycodone (5 mg) ratings of "high" were potentiated by 5 mg dronabinol (p < 0.05; placebo = 1.1 [± 0.7]; 5 mg oxycodone = 4.7 [± 2.2]; 5 mg dronabinol = 9.9 [± 8.4]; 5 mg oxycodone + 5 mg dronabinol = 37.4 [± 11.3]).This study indicates that dronabinol did not enhance the analgesic effects of oxycodone and increased abuse- and impairment-related subjective effects. These data suggest that dronabinol may not be an effective or appropriate opioid adjuvant; it could potentially increase opioid dose requirements, while increasing psychoactive opioid effects.CONCLUSIONSThis study indicates that dronabinol did not enhance the analgesic effects of oxycodone and increased abuse- and impairment-related subjective effects. These data suggest that dronabinol may not be an effective or appropriate opioid adjuvant; it could potentially increase opioid dose requirements, while increasing psychoactive opioid effects. |
| Audience | Academic |
| Author | Fanucchi, Laura C. Sloan, Paul A. Walsh, Sharon L. Lofwall, Michelle R. Babalonis, Shanna Nuzzo, Paul A. |
| AuthorAffiliation | 3 Department of Anesthesiology, University of Kentucky, College of Medicine, Lexington, KY 2 Center on Drug and Alcohol Research, University of Kentucky, College of Medicine, Lexington, KY 5 Department of Internal Medicine, University of Kentucky, College of Medicine, Lexington, KY 4 Department of Psychiatry, University of Kentucky, College of Medicine, Lexington, KY 1 Department of Behavioral Science, University of Kentucky, College of Medicine, Lexington, KY |
| AuthorAffiliation_xml | – name: 3 Department of Anesthesiology, University of Kentucky, College of Medicine, Lexington, KY – name: 1 Department of Behavioral Science, University of Kentucky, College of Medicine, Lexington, KY – name: 4 Department of Psychiatry, University of Kentucky, College of Medicine, Lexington, KY – name: 5 Department of Internal Medicine, University of Kentucky, College of Medicine, Lexington, KY – name: 2 Center on Drug and Alcohol Research, University of Kentucky, College of Medicine, Lexington, KY |
| Author_xml | – sequence: 1 givenname: Shanna orcidid: 0000-0002-1450-2621 surname: Babalonis fullname: Babalonis, Shanna email: babalonis@uky.edu organization: Department of Behavioral Science, University of Kentucky College of Medicine, Center on Drug and Alcohol Research, University of Kentucky College of Medicine – sequence: 2 givenname: Michelle R. surname: Lofwall fullname: Lofwall, Michelle R. organization: Department of Behavioral Science, University of Kentucky College of Medicine, Center on Drug and Alcohol Research, University of Kentucky College of Medicine, Department of Psychiatry, University of Kentucky College of Medicine – sequence: 3 givenname: Paul A. surname: Sloan fullname: Sloan, Paul A. organization: Department of Anesthesiology, University of Kentucky College of Medicine – sequence: 4 givenname: Paul A. surname: Nuzzo fullname: Nuzzo, Paul A. organization: Center on Drug and Alcohol Research, University of Kentucky College of Medicine – sequence: 5 givenname: Laura C. surname: Fanucchi fullname: Fanucchi, Laura C. organization: Center on Drug and Alcohol Research, University of Kentucky College of Medicine, Department of Internal Medicine, University of Kentucky College of Medicine – sequence: 6 givenname: Sharon L. surname: Walsh fullname: Walsh, Sharon L. organization: Department of Behavioral Science, University of Kentucky College of Medicine, Center on Drug and Alcohol Research, University of Kentucky College of Medicine, Department of Psychiatry, University of Kentucky College of Medicine |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31201479$$D View this record in MEDLINE/PubMed |
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| Issue | 11 |
| Keywords | Human Opioid Pain Opioid sparing Cannabinoid Dronabinol |
| Language | English |
| License | Terms of use and reuse: academic research for non-commercial purposes, see here for full terms. http://www.springer.com/gb/open-access/authors-rights/aam-terms-v1 |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 ObjectType-Undefined-3 Shanna Babalonis, Michelle Lofwall, Paul Sloan and Sharon Walsh were responsible for the study concept and design. Shanna Babalonis directly supervised the conduct of the study, interviewed and consented the participants, directed the statistical analyses and wrote the manuscript. Michelle Lofwall and Laura Fanucchi conducted medical interviews, physical examinations and reviewed laboratory results. Michelle Lofwall, Paul Sloan and Laura Fanucchi provided medical coverage and edited the manuscript. Paul Nuzzo trained the staff, provided technical support services, supervised daily operations and conducted data analyses. Sharon Walsh, Michelle Lofwall, Paul Sloan, Laura Fanucchi and Paul Nuzzo provided critical revisions of the manuscript for important intellectual content. Author Contributions |
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| PublicationTitle | Psychopharmacology |
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| Publisher | Springer Berlin Heidelberg Springer Springer Nature B.V |
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Dozens of preclinical studies have reported cannabinoid agonist potentiation of the analgesic effects of μ-opioid agonists.
Objectives
The aim of... Dozens of preclinical studies have reported cannabinoid agonist potentiation of the analgesic effects of μ-opioid agonists. The aim of this study was to... Rationale Dozens of preclinical studies have reported cannabinoid agonist potentiation of the analgesic effects of [mu]-opioid agonists. Objectives The aim of... Dozens of preclinical studies have reported cannabinoid agonist potentiation of the analgesic effects of [mu]-opioid agonists. The aim of this study was to... RationaleDozens of preclinical studies have reported cannabinoid agonist potentiation of the analgesic effects of μ-opioid agonists.ObjectivesThe aim of this... Dozens of preclinical studies have reported cannabinoid agonist potentiation of the analgesic effects of μ-opioid agonists.RATIONALEDozens of preclinical... |
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| SubjectTerms | Abuse Adolescent Adult Agonists Analgesia Analgesia - methods Analgesia - psychology Analgesics Analgesics, Opioid - pharmacology Analgesics, Opioid - therapeutic use Analysis Biomedical and Life Sciences Biomedicine Blindness Cannabinoid Receptor Agonists - pharmacology Cannabinoid Receptor Agonists - therapeutic use Cannabinoid receptors Cold tolerance Cross-Over Studies Diagnostic Self Evaluation Double-Blind Method Drug dosages Drug tolerance Female Healthy Volunteers Humans Hyperalgesia Male Middle Aged Narcotics Neurosciences Opioids Original Investigation Oxycodone Pain Pain - drug therapy Pain - psychology Pain Measurement - drug effects Pain Measurement - methods Pain Measurement - psychology Pain perception Pharmacology/Toxicology Pressure Pressure tolerance Psychiatry Psychomotor Performance - drug effects Psychomotor Performance - physiology Remifentanil Tetrahydrocannabinol Young Adult |
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| Title | Cannabinoid modulation of opioid analgesia and subjective drug effects in healthy humans |
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