Duluth Medical Research Institute, University of Minnesota Medical School, Duluth, MN 55812, USA.
Biol Psychol. 2013 Apr;93(1):1-8. doi: 10.1016/j.biopsycho.2012.12.007. Epub 2012 Dec 26.
Alterations in the stress response and endogenous pain regulation mechanisms may contribute directly and indirectly to maintenance of nicotine dependence and relapse. We examined the extent to which nicotine dependence alters endogenous pain regulatory systems, including the hypothalamic-pituitary-adrenocortical axis, cardiovascular activity, and stress-induced analgesia. Smokers and nonsmokers attended a laboratory session that included assessment of hormonal and cardiovascular responses to stress. Smokers smoked at their regular rate prior to the session. The hand cold pressor and heat thermal pain tests were completed twice, once after acute stress (public speaking and math tasks) and the other after rest. While smokers and nonsmokers exhibited significant hormonal and cardiovascular responses to stress, smokers exhibited blunted stress responses relative to nonsmokers. They also exhibited diminished stress-induced analgesia. Results demonstrate altered stress response and diminished stress-induced analgesia among chronic smokers, and suggest that these dysregulated physiological responding may contribute to altered endogenous pain regulation.
应激反应和内源性疼痛调节机制的改变可能直接或间接导致尼古丁依赖和复吸的维持。我们研究了尼古丁依赖改变内源性疼痛调节系统的程度,包括下丘脑-垂体-肾上腺皮质轴、心血管活动和应激诱导的镇痛。吸烟者和不吸烟者参加了一个实验室会议,包括评估应激时的激素和心血管反应。吸烟者在会议前按正常速度吸烟。进行了两次手部冷加压和热痛觉测试,一次在急性应激(公开演讲和数学任务)后,另一次在休息后。虽然吸烟者和不吸烟者对压力表现出明显的激素和心血管反应,但与不吸烟者相比,吸烟者的应激反应减弱。他们还表现出应激诱导的镇痛作用减弱。结果表明,慢性吸烟者的应激反应改变和应激诱导的镇痛作用减弱,这表明这些失调的生理反应可能导致内源性疼痛调节的改变。