CAFFEINE AND CARDIOVASCULAR RESPONSES TO STRESS

咖啡因和压力有一定的心血管（CV）和神经内分泌（NE） 共同的影响，这表明咖啡因可以增加或加强 CV和NE对应激的反应可能具有病理学影响，导致 CV疾病。 这项研究计划的长期目标是 CV和NE的潜在咖啡因应激相互作用的研究 应答 我们已经证明，咖啡因可以增加或放大CV反应 压力 我们提出三个新问题， 咖啡因-压力相互作用：咖啡因是否也能增强NE对 压力？ 习惯性使用咖啡因的模式是否会影响 咖啡因的CV和NE效应（是否产生耐受性）？ 尼古丁是否 与咖啡因和压力相互作用，产生更大的CV和NE 反应与病理学的影响。 三项研究中的第一项将 检查咖啡因对CV和NE（儿茶酚胺和 皮质醇）对实验室心理压力的反应。 心率， 将测量血压和骨骼肌血管活性， 在休息和实验应激条件下采集的血样， 两次服用咖啡因或安慰剂。 第二 这项研究将评估咖啡因对相同条件下CV和NE活性的影响。 受试者在正常的一天的活动。 门诊措施 心率和血压以及尿排泄的测量 将在受试者中采集儿茶酚胺和皮质醇， 给予咖啡因或安慰剂。 在这两项研究中，我们将研究 咖啡因影响的程度是否与习惯模式有关 通过一周的摄入日记来评估咖啡因的使用。 在第三项研究中， 尼古丁、咖啡因及其组合的影响将在一个 四个阶段，安慰剂对照设计，其中静息时CV和NE活性 和在应力期间，如在研究1中测量。 这些研究将帮助我们 了解咖啡因对压力的影响机制，将决定 是否耐受这些影响出现与定期使用咖啡因， 尼古丁和咖啡因，在社会上被广泛使用， 联合收割机进一步加强CV和NE对应激的反应。 这些知识 将有助于澄清咖啡因消费可能在 心血管疾病的发病机制。

Caffeine and stress have some cardiovascular (CV) and neuroendocrine (NE) effects in common which suggests that caffeine could augment or intensify CV and NE responses to stress which may have pathological effects leading to CV disease. The long-term objectives of this research program are the investigation of potential caffeine-stress interactions for CV and NE responses. We have shown that caffeine can add to or magnify CV responses to stress. We propose to address three new questions concerning caffeine-stress interactions: Can caffeine also intensify NE responses to stress? Do patterns of habitual caffeine use influence the magnitude of caffeine's CV and NE effects (Does tolerance develop)? and Does nicotine interact with caffeine and stress to produce even greater CV and NE responses with implications for pathology. The first of three studies will examine the effects of caffeine on both CV and NE (catecholamine and cortisol) responses to psychological stress in the lboratory. Heart rate, blood pressure, and skeletal muscle vasomotor activity will be measured and samples of blood drawn under conditions of rest and experimental stress in two sessions in which caffeine or placebo is administered. The second study will assess the effects of caffeine on CV and NE activity in the same subjects during the activities of the normal day. Ambulatory measures of heart rate and blood pressure and measures of urinary excretion of catecholamines and cortisol will be obtained from subjects on days in which caffeine or placebo are administered. In both studies, we will examine whether the magnitude of caffeine effects is related to habitual patterns of caffeine use assessed by a 1-week intake diary. In the third study, the effects of nicotine, caffeine and their combination will be assessed in a four session, placebo controlled design in which CV and NE activity at rest and during stress are measured as in Study 1. These studies will help us understand the mechanisms of caffeine's effects on stress, will determine whether tolerance to these effects appears with regular caffeine use, and whether nicotine and caffeine, so commonly used together in society, combine to further intensify CV and NE responses to stress. This knowledge will help to clarify the role which caffeine consumption may have in the pathogenesis of cardiovascular disease.