Rose Jed E, Brauer Lisa H, Behm Frederique M, Cramblett Matthew, Calkins Kevin, Lawhon Dawn
VA Medical Center and Department of Psychiatry, Duke University Medical Center, Durham, NC, USA.
Nicotine Tob Res. 2004 Feb;6(1):133-44. doi: 10.1080/14622200310001656957.
Epidemiological, clinical, and laboratory evidence has shown a positive correlation between cigarette smoking and ethanol use, and previous studies suggest some commonality in the neural pathways mediating effects of nicotine and ethanol. In this study, the subjective and behavioral interactions among nicotine, ethanol, and the nicotinic antagonist mecamylamine were investigated. The main objectives were to determine how the rewarding effects of nicotine might be modified by ethanol, and to compare the effects of ethanol with those of a nicotinic antagonist (mecamylamine). A total of 48 smokers who regularly consumed alcoholic beverages participated in four laboratory sessions presenting a 2 (nicotine vs. denicotinized cigarette smoke)x2 (10 mg oral mecamylamine hydrochloride vs. placebo)x2 (ethanol.5 g/kg vs. placebo) design, with ethanol as a between-subjects factor. Dependent measures included blood alcohol concentration (BAC), as assessed by breath alcohol detector; subjective drug effects; and rate of ad lib smoking during a 2-hr period. Results showed that peak BAC averaged.03 g/dl in the ethanol condition. Ethanol potentiated some of the subjective rewarding effects of nicotine, including smoking satisfaction, stimulant as well as calming effects, and relief of craving for cigarettes. During the ad lib smoking period, mecamylamine decreased satisfaction associated with the nicotine-containing cigarettes; mecamylamine also induced smoking but only in the placebo ethanol condition. These results highlight the potent interaction between ethanol and nicotinic systems, and suggest that ethanol can potentiate the rewarding effects of nicotine as well as offset some of the effects of a nicotinic antagonist.
流行病学、临床和实验室证据表明,吸烟与饮酒之间存在正相关,并且先前的研究表明,在介导尼古丁和乙醇作用的神经通路中存在一些共性。在本研究中,对尼古丁、乙醇和烟碱拮抗剂美加明之间的主观和行为相互作用进行了研究。主要目的是确定乙醇如何改变尼古丁的奖赏效应,并将乙醇的效应与烟碱拮抗剂(美加明)的效应进行比较。共有48名经常饮用酒精饮料的吸烟者参加了四个实验室环节,采用2(尼古丁与去尼古丁香烟烟雾)×2(10毫克口服盐酸美加明与安慰剂)×2(乙醇0.5克/千克与安慰剂)设计,乙醇作为组间因素。相关测量指标包括通过呼气酒精探测器评估的血液酒精浓度(BAC)、主观药物效应以及2小时内的自由吸烟率。结果显示,在乙醇条件下,BAC峰值平均为0.03克/分升。乙醇增强了尼古丁的一些主观奖赏效应,包括吸烟满意度、兴奋以及镇静作用,以及减轻对香烟的渴望。在自由吸烟期间,美加明降低了与含尼古丁香烟相关的满意度;美加明还诱导了吸烟,但仅在安慰剂乙醇条件下。这些结果突出了乙醇与烟碱系统之间的强大相互作用,并表明乙醇可以增强尼古丁的奖赏效应,以及抵消烟碱拮抗剂的一些效应。