Caffeine and theophylline attenuate adenosine‐induced vasodilation in humans

Caffeine and theophylline attenuate adenosine‐induced vasodilation in humans
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咖啡因和茶碱可减弱腺苷引起的人体血管舒张

DOI:
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发表时间:
1990
期刊:
Clinical pharmacology and therapy
影响因子:
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通讯作者:
T. Thien
T. Thien
中科院分区:
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文献类型:
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作者:
P. Smits;J. Lenders;T. Thien

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在这项研究中,我们探讨了腺苷在人体前臂的局部血管活性作用。将腺苷(15μg/100ml前臂/分钟)注入臂动脉(n=6),前臂血流量增加572%±140%,而安慰剂组−增加0.5%±5.8%(p<0.01)。较低的腺苷输注速率(5μg/100ml前臂/分钟,3次)可使前臂血流量分别增加330%±94%、339%±67%和330%±79%(n=8)。同时动脉注射咖啡因(30和90μg/100ml前臂/分钟),前臂血流反应分别降低到150%±45%和98%±28%。茶碱(30μg/100ml前臂/分钟;n=6)也能显著减弱腺苷引起的前臂血流量增加。体外与腺苷受体亲和力较低的黄嘌呤(30μg/100ml前臂/分钟)不改变对腺苷的反应。与安慰剂相比,咖啡因对硝普钠(50 ng/100ml前臂/分钟)的非特异性血管扩张无抑制作用(前臂血流反应分别为202%±21%和216%±40%;n=6)。这项研究表明,咖啡因和茶碱能特异性地减少腺苷诱导的人类血管扩张,支持存在功能性的人类血管腺苷受体。
In this study the local vasoactive effects of adenosine were explored in the human forearm. Adenosine (15 μg/100 ml forearm/min) infused into the brachial artery (n = 6) increased forearm blood flow by 572% ± 140%, versus −0.5% ± 5.8% during placebo infusion (p < 0.01). Lower adenosine infusion rates (5 μg/100 ml forearm/min, three times) induced forearm blood flow increments to 330% ± 94%, 339% ± 67% and 330% ± 79%, respectively (n = 8). These forearm blood flow responses were reduced (p = 0.02) during concomitant intra‐arterial infusion of two doses of caffeine (30 and 90 μg/100 ml forearm/min) to 150% ± 45% and 98% ± 28%, respectively. Theophylline (30 μg/100 ml forearm/min; n = 6) also significantly attenuated the adenosine‐induced increase in forearm blood flow. Enprofylline (30 μg/100 ml forearm/min), a related xanthine with a low affinity to adenosine receptors in vitro, did not change the response to adenosine. Nonspecific vasodilation by sodium nitroprusside infusion (50 ng/100 ml forearm/min) was not inhibited by caffeine compared with placebo (forearm blood flow responses were 202% ±21% versus 216% ± 40%; n = 6). This study demonstrated that caffeine and theophylline specifically reduce adenosine‐induced vasodilation in humans, supporting the existence of functional human vascular adenosine receptors.