ELEVATED ENDOTHELIN-1 LEVELS AFTER CIGARETTE-SMOKING

ELEVATED ENDOTHELIN-1 LEVELS AFTER CIGARETTE-SMOKING
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DOI:
10.1016/0026-0495(94)90091-4
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发表时间:
1994-03-01
影响因子:
9.8
通讯作者:
USADEL, KH
USADEL, KH
中科院分区:
医学1区
文献类型:
--
作者:
HAAK, T;JUNGMANN, E;USADEL, KH

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本文研究了10例男性健康吸烟者短期尼古丁摄入量对血浆内皮素-1(ET-1)水平的影响。志愿者随机分3天抽一支低焦油香烟或一支高焦油香烟,或者被研究人员不吸烟(无烟实验)。分别于吸烟前、吸烟后1分钟、3分钟、5分钟、10分钟、20分钟和30分钟测定ET-1、促肾上腺皮质激素、皮质醇水平、心率和血压。与吸低焦油香烟或不吸烟的结果相反,吸烟高焦油香烟会导致ET-1水平在10分钟内显著升高,随后在吸烟后20分钟内促肾上腺皮质激素水平升高。吸烟30分钟后,与低焦油香烟或不吸烟相比,高焦油香烟的皮质醇水平更高。同样,吸高焦油香烟后的心率和收缩压的增加也比吸低焦油香烟后的高。综上所述,我们很容易推测,ET-1可能确实在加压素和促肾上腺皮质激素释放激素(CRH)之间扮演了人们长期寻找的纽带,从而在刺激下丘脑-垂体-肾上腺轴方面发挥了重要作用。此外,这些结果提示,ET-1是一种强大的血管收缩和丝裂原,其水平的升高可能在吸烟引起的动脉粥样硬化的发病机制中发挥重要作用。
The effect of short-term nicotine consumption on endothelin-1 (ET-1) levels was studied in 10 male healthy smokers. Volunteers smoked in random order on 3 separate days a low-tar cigarette or a high-tar cigarette, or were studied without having smoked (no-cigarette experiment). ET-1, corticotropin, and cortisol levels, heart rate, and blood pressure were determined before and 1, 3, 5, 10, 20, and 30 minutes after smoking. In contrast to results obtained after smoking a low-tar cigarette or not smoking, smoking a high-tar cigarette resulted in a significant increase in ET-1 levels within 10 minutes, followed by an increase in corticotropin levels within 20 minutes after smoking. Thirty minutes after smoking, cortisol levels were higher after a high-tar cigarette compared with a low-tar cigarette or no smoking. Increases in heart rate and systolic blood pressure were likewise higher after smoking a high-tar cigarette than after smoking a low-tar cigarette. In conclusion, it is tempting to speculate that ET-1 may indeed act as the long-searched-for link between vasopressin and corticotropin-releasing hormone (CRH) and thus play an essential role in the stimulation of the hypothalamic-pituitary-adrenal axis. In addition, these results suggest that the increase in the level of ET-1, a powerful vasoconstrictor and mitogen, may play an important part in the disease mechanisms of atherosclerosis arising from smoking.