Smith Andrew, Brice Carolyn, Nash Jon, Rich Neil, Nutt David J
Centre for Occupational and Health Psychology, School of Psychology, Cardiff University, Cardiff, UK.
J Psychopharmacol. 2003 Sep;17(3):283-92. doi: 10.1177/02698811030173010.
There have been numerous studies on the effects of caffeine on behaviour and cardiovascular function. It is now important to clarify the mechanisms that underlie such effects, and the main objective of the present study was to investigate whether changes in central noradrenaline underlie some of the behavioural and cardiovascular effects of caffeine. This was examined using a clonidine challenge paradigm. Twenty-four healthy volunteers were assigned to one of four conditions: (i) clonidine/caffeine; (ii) clonidine/placebo; (iii) placebo/caffeine: (iv) placebo/placebo. Baseline measurements of mood, cognitive performance, saccadic eye movements and cardiovascular function were recorded. Subsequently, volunteers were given either clonidine (200 microg) or placebo and consumed coffee containing caffeine (1.5 mg/kg) or placebo. The test battery was then repeated 30 min, 150 min and 270 min later. A second cup of coffee (with the same amount of caffeine as the first) was consumed 120 min after the first cup. The results showed that clonidine reduced alertness, impaired many aspects of performance and slowed saccadic eye movements; caffeine removed many of these impairments. Both clonidine and caffeine influenced blood pressure (clonidine reduced it, caffeine raised it) but the effects appeared to be independent, suggesting that separate mechanisms were involved. In addition, there were some behavioural effects of caffeine that were independent of the clonidine effect (e.g. effects on speed of encoding of new information) and these may reflect other neurotransmitter systems (e.g cholinergic effects). Overall, the results suggest that caffeine counteracts reductions in the turnover of central noradrenaline. This mechanism may underlie the beneficial effects of caffeine seen in low alertness states.
关于咖啡因对行为和心血管功能的影响,已经有大量研究。现在,阐明这些影响背后的机制很重要,本研究的主要目的是调查中枢去甲肾上腺素的变化是否是咖啡因某些行为和心血管效应的基础。这是通过可乐定激发范式进行研究的。24名健康志愿者被分配到以下四种情况之一:(i)可乐定/咖啡因;(ii)可乐定/安慰剂;(iii)安慰剂/咖啡因;(iv)安慰剂/安慰剂。记录了情绪、认知表现、眼球快速运动和心血管功能的基线测量值。随后,志愿者们被给予可乐定(200微克)或安慰剂,并饮用含咖啡因(1.5毫克/千克)或安慰剂的咖啡。然后在30分钟、150分钟和270分钟后重复进行测试。在第一杯咖啡饮用120分钟后,饮用第二杯咖啡(咖啡因含量与第一杯相同)。结果表明,可乐定降低了警觉性,损害了许多方面的表现,并减缓了眼球快速运动;咖啡因消除了许多这些损害。可乐定和咖啡因都影响血压(可乐定使其降低,咖啡因使其升高),但这些影响似乎是独立的,这表明涉及不同的机制。此外,咖啡因有一些行为效应独立于可乐定的效应(例如对新信息编码速度的影响),这些可能反映了其他神经递质系统(例如胆碱能效应)。总体而言,结果表明咖啡因抵消了中枢去甲肾上腺素周转率的降低。这种机制可能是低警觉状态下咖啡因有益作用的基础。