UCLA Center for Cannabis and Cannabinoids, Jane and Terry Semel Institute for Neuroscience and Human Behavior, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles, USA.
Columbia University Irving Medical Center, New York State Psychiatric Institute, 1051 Riverside Drive, New York, NY, USA.
Drug Alcohol Depend. 2023 Feb 1;243:109757. doi: 10.1016/j.drugalcdep.2022.109757. Epub 2022 Dec 29.
Despite the high prevalence of polysubstance use, outcomes and potential risks associated with common drug combinations are not well characterized. Many individuals who use cocaine also use cannabis, yet little is known about how interactions between the two drugs might contribute to continued co-use.
The aim of this double-blind, placebo-controlled study was to determine the physiological and subjective effects of smoked cannabis with smoked cocaine, to identify variables that may contribute to the continued use of this drug combination. Healthy, non-treatment seeking volunteers who reported smoking both cocaine and cannabis (N = 9, all males) completed a 13-day inpatient protocol. On session days, cannabis [0.0 or 5.6 % tetrahydrocannabinol (THC)] was administered 28 min prior to cocaine (0, 12, or 25 mg). Dependent measures included pharmacokinetic assessment of THC and cocaine and their respective metabolites, in addition to subjective and cardiovascular effects.
Active cannabis (5.6 % THC) increased plasma levels of THC and the metabolite 11-nor-9-carboxy-Δ9-THC (THCCOOH), as well as subjective ratings of cannabis effects and heart rate relative to inactive cannabis. Cocaine dose-dependently increased plasma cocaine and metabolites and subjective ratings of cocaine effects. Active cannabis pre-treatment decreased plasma levels of cocaine and metabolites. Furthermore, active cannabis attenuated cocaine-related reductions in 'Hunger' and 'Calm.'
Cannabis pre-treatment altered the subjective experience of smoked cocaine and reduced peak plasma levels of cocaine. Future studies should explore additional doses of each drug and whether these changes also impact cocaine's reinforcing effects.
尽管多种物质使用的患病率很高,但与常见药物组合相关的结果和潜在风险仍未得到很好的描述。许多使用可卡因的人也使用大麻,但人们对这两种药物之间的相互作用如何导致持续共同使用知之甚少。
本双盲、安慰剂对照研究的目的是确定吸食大麻和吸食可卡因的生理和主观影响,确定可能导致这种药物组合持续使用的变量。报告吸食可卡因和大麻的健康、未接受治疗的志愿者(N=9,均为男性)完成了 13 天的住院方案。在会议日,大麻(0.0 或 5.6%四氢大麻酚(THC))在可卡因(0、12 或 25mg)给药前 28 分钟给予。依赖措施包括 THC 和可卡因及其各自代谢物的药代动力学评估,以及主观和心血管效应。
活性大麻(5.6%THC)增加了 THC 和代谢物 11-去甲-9-羧基-Δ9-THC(THCCOOH)的血浆水平,以及大麻效应和心率的主观评分,与非活性大麻相比。可卡因剂量依赖性地增加了血浆可卡因及其代谢物和可卡因效应的主观评分。活性大麻预处理降低了可卡因和代谢物的血浆水平。此外,活性大麻减轻了与可卡因相关的“饥饿”和“平静”的减少。
大麻预处理改变了吸食可卡因的主观体验,并降低了可卡因的峰值血浆水平。未来的研究应该探索每种药物的其他剂量,以及这些变化是否也会影响可卡因的强化作用。