CAFFEINE AND CARDIOVASCULAR RESPONSES TO STRESS

咖啡因和应激有一定的心血管(CV)和神经内分泌(NE)。 共同的影响，这表明咖啡因可以增强或增强 心血管和去甲肾上腺素对压力的反应可能具有病理效应 与心血管疾病有关。这项研究计划的长期目标是 咖啡因-应激对血管紧张素和去甲肾上腺素潜在相互作用的研究 回应。我们已经证明，咖啡因可以增加或放大CV反应 来施加压力。我们建议解决关于以下三个新问题 咖啡因-应激相互作用：咖啡因是否也能增强NE对 压力？习惯性使用咖啡因的方式是否会影响 咖啡因的CV和NE效应(是否会产生耐受性)？尼古丁是否会 与咖啡因和压力相互作用，产生更大的CV和NE 对病理学有影响的反应。三项研究中的第一项将 研究咖啡因对心血管和NE(儿茶酚胺和肾上腺素)的影响 皮质醇)对呼吸中的心理压力的反应。心率, 血压和骨骼肌血管运动活性将被测量和 静息状态和实验应激状态下采集的血液样本 两次服用咖啡因或安慰剂。第二 研究将评估咖啡因对脑循环和去甲肾上腺素活动的影响。 受试者在正常一天的活动中。不定期的措施 心率、血压和尿液排泄量 儿茶酚胺和皮质醇将在下列日期从受试者中获得 服用咖啡因或安慰剂。在这两项研究中，我们将检查 咖啡因效应的大小是否与习惯模式有关 通过一周的摄入日记评估咖啡因的使用情况。在第三项研究中， 尼古丁、咖啡因及其组合的影响将在一项 四个疗程，安慰剂对照设计，其中CV和NE在休息时活动 和研究1一样测量压力。这些研究将帮助我们 了解咖啡因对压力的影响机制，将确定 经常使用咖啡因是否会出现对这些影响的耐受性，以及 无论是尼古丁和咖啡因，在社会上经常一起使用， 结合在一起，进一步加强CV和NE对应激的反应。这一知识 将有助于澄清咖啡因摄取可能在 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.