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兴奋剂导致吸烟量增加的药理学分析。

A pharmacological analysis of stimulant-induced increases in smoking.

作者信息

Vansickel Andrea R, Stoops William W, Glaser Paul E A, Rush Craig R

机构信息

Department of Behavioral Science, College of Medicine, University of Kentucky, Lexington, KY 40536, USA.

出版信息

Psychopharmacology (Berl). 2007 Aug;193(3):305-13. doi: 10.1007/s00213-007-0786-z. Epub 2007 Apr 20.

DOI:10.1007/s00213-007-0786-z
PMID:17447052
Abstract

RATIONALE

Stimulants increase tobacco smoking in healthy adults under controlled laboratory conditions. The mechanisms that mediate stimulant-induced increases in smoking are not known.

OBJECTIVE

The purpose of the present experiment was to characterize the pharmacological specificity of stimulant-induced increases in smoking. We tested the effects of methylphenidate and atomoxetine on smoking behavior. Atomoxetine is a norepinephrine transport inhibitor that does not increase dopamine levels in the nucleus accumbens or striatum. If stimulant-induced increases in smoking result from an additive or synergistic effect of these drugs and nicotine on dopamine levels in the nucleus accumbens or striatum, methylphenidate but not atomoxetine should increase smoking.

MATERIALS AND METHODS

Doses of methylphenidate (10, 20, and 40 mg) and atomoxetine (20, 40, and 80 mg) were tested once while placebo was tested twice in 12 cigarette smokers. One hour after ingesting drug, participants smoked ad libitum for 4 h. Measures of smoking included total cigarettes, total puffs, and carbon monoxide levels. Snacks and decaffeinated drinks were available ad libitum, and food intake was calculated.

RESULTS

Methylphenidate but not atomoxetine dose-dependently increased the number of cigarettes, puffs, and carbon monoxide levels. Methylphenidate and atomoxetine decreased food intake.

CONCLUSIONS

The results of this experiment are consistent with the notion that stimulant-induced increases in smoking may result from an additive or synergistic effect of these drugs and nicotine on dopamine levels in the nucleus accumbens or striatum. Additional research is needed to more fully understand the pharmacological mechanisms that mediate the relationship between stimulant use and smoking.

摘要

理论依据

在可控的实验室条件下,兴奋剂会增加健康成年人的吸烟量。介导兴奋剂导致吸烟量增加的机制尚不清楚。

目的

本实验的目的是确定兴奋剂导致吸烟量增加的药理学特异性。我们测试了哌甲酯和托莫西汀对吸烟行为的影响。托莫西汀是一种去甲肾上腺素转运抑制剂,不会增加伏隔核或纹状体中的多巴胺水平。如果兴奋剂导致的吸烟量增加是这些药物与尼古丁对伏隔核或纹状体中多巴胺水平产生相加或协同作用的结果,那么哌甲酯会增加吸烟量,而托莫西汀则不会。

材料与方法

对12名吸烟者测试了哌甲酯(10、20和40毫克)和托莫西汀(20、40和80毫克)的剂量,每种剂量测试一次,而安慰剂测试两次。服药1小时后,参与者自由吸烟4小时。吸烟量的测量指标包括香烟总数、总吸数和一氧化碳水平。随时提供零食和无咖啡因饮料,并计算食物摄入量。

结果

哌甲酯而非托莫西汀剂量依赖性地增加了香烟数量、吸数和一氧化碳水平。哌甲酯和托莫西汀均降低了食物摄入量。

结论

本实验结果与以下观点一致,即兴奋剂导致的吸烟量增加可能是这些药物与尼古丁对伏隔核或纹状体中多巴胺水平产生相加或协同作用的结果。需要进行更多研究以更全面地了解介导兴奋剂使用与吸烟之间关系的药理学机制。

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