Effects of acute administration of caffeine on vascular function

Effects of acute administration of caffeine on vascular function
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DOI:
10.1016/j.amjcard.2006.06.058
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发表时间:
2006-12-01
影响因子:
2.8
通讯作者:
Higashi, Yukihito
Higashi, Yukihito
中科院分区:
医学3区
文献类型:
--
作者:
Umemura, Takashi;Ueda, Keiko;Higashi, Yukihito

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咖啡因是世界上使用最广泛的药理物质。它存在于常见的非必需品中(如咖啡、茶、可可和巧克力)。咖啡因对包括高血压在内的心血管疾病的影响仍然存在争议,关于其对血管功能的直接影响的信息也很少。这项研究的目的是确定咖啡因对人类内皮功能的影响。该研究是一项双盲、随机、安慰剂和活性药物研究。观察了健康青年人口服咖啡因300 mg(n=10)或安慰剂(n=10)前后前臂血流(FBF)对血管内皮依赖性药物乙酰胆碱(ACh)和非内皮依赖性血管扩张剂硝普钠(Nitprusside)的反应。用应变片体积描记仪测量FBF。咖啡因使收缩压和舒张压分别显著增加6.0+/-6.0和2.6+/-3.1毫米汞柱(p<0.05),但不改变心率或基线空腹血糖。咖啡因使FBF对ACh的反应从21.2+/-7.1增加到26.6+/-8.1ml/min/100ml组织(p<0.05),而硝普钠刺激的血管扩张不受咖啡因的影响。动脉内注入一氧化氮合酶抑制剂N-G-单甲基-L-精氨酸可阻断咖啡因引起的FBF对ACh反应的增强。在安慰剂组,ACh和硝普钠刺激的血管扩张在随访期前后相似。总而言之,这些发现表明,急性服用咖啡因通过增加一氧化氮的产生,增强了健康年轻男性的内皮依赖性血管扩张。(C)2006 Elsevier Inc.保留所有权利。
Caffeine is the most widely used pharmacologic substance in the world. It is found in common nonessential grocery items (e.g., coffee, tea, cocoa, and chocolate). The effects of caffeine on cardiovascular diseases, including hypertension, remain controversial, and there is little information on its direct effect on vascular function. The purpose of this study was to determine the effect of caffeine on endothelial function in humans. This study was a double-blind, randomized placebo and active drug study. Forearm blood flow (FBF) responses to acetylcholine (ACh), an endothelium-dependent vasodilator, and to sodium nitroprusside, an endothelium-independent vasodilator, were evaluated in healthy young men before and after the oral administration of caffeine 300 mg (n = 10) or placebo (n = 10). FBF was measured by using a strain-gauge plethysmograph. Caffeine significantly increased systolic and diastolic blood pressures by 6.0 +/- 6.0 and 2.6 +/- 3.1 mm Hg (p < 0.05), respectively, but did not alter heart rate or baseline FBF. Caffeine augmented the FBF responses to ACh from 21.2 +/- 7.1 to 26.6 +/- 8.1 ml/min/100 ml tissue (p < 0.05), whereas sodium nitroprusside-stimulated vasodilation was not altered by caffeine administration. The intra-arterial infusion of N-G-monomethyl-L-arginine, a nitric oxide synthase inhibitor, abolished the caffeine-induced augmentation of FBF response to ACh. In the placebo group, the ACh- and sodium nitroprusside-stimulated vasodilation was similar before and after the follow-up period. In conclusion, these findings suggest that the acute administration of caffeine augments endothelium-dependent vasodilation in healthy young men through an increase in nitric oxide production. (c) 2006 Elsevier Inc. All rights reserved.