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在人体持续输注血管紧张素II和地塞米松的情况下,依他尼酸诱导急性容量耗竭对血浆醛固酮、肾素活性和皮质醇的影响。

Effect on plasma aldosterone, renin activity and cortisol of acute volume depletion induced by ethacrynic acid under constant infusion of angiotensin II and dexamethasone in man.

作者信息

Gaillard R C, Merkelbach U, Riondel A M, Vallotton M B, Muller A F

出版信息

Eur J Clin Invest. 1976 Jan 30;6(1):51-7. doi: 10.1111/j.1365-2362.1976.tb00493.x.

Abstract

The influence on plasma aldosterone of acute volume depletion induced by ethacrynic acid was studied in man. The experiments were performed during the morning in supine healthy males receiving a control infusion of 5% glucose or an infusion of angiotensin II (AII) to suppress endogenous renin production or an infusion of dexamethasone to suppress endogenous ACTH. Ethacrynic acid induced in all circumstances a similar diuresis and volume depletion. The rise of plasma renin activity (PRA) was effectively suppressed by AII and the rise of plasma cortisol by dexamethasone. Plasma aldosterone (PA) rose markedly even when the elevation of PRA or cortisol were suppressed. Yet when both endogenous renin and ACTH secretion were blocked, PA rose much less after ethacrynic acid. This residual increase could be attributed mainly to a decrease of the metabolic clearance rate (MCR) of aldosterone which had been measured before and after ethacrynic acid administration. The data presented indicate that multiple factors influencing PA after acute volume depletion could be dissected out and that renin, ACTH and a decrease of the MCR each contribute to the elevation of PA.

摘要

在人体中研究了依他尼酸诱导的急性容量耗竭对血浆醛固酮的影响。实验于早晨在仰卧位的健康男性中进行,这些男性接受5%葡萄糖的对照输注,或输注血管紧张素II(AII)以抑制内源性肾素的产生,或输注地塞米松以抑制内源性促肾上腺皮质激素(ACTH)。在所有情况下,依他尼酸都引起相似的利尿和容量耗竭。AII有效抑制了血浆肾素活性(PRA)的升高,地塞米松抑制了血浆皮质醇的升高。即使PRA或皮质醇的升高受到抑制,血浆醛固酮(PA)仍显著升高。然而,当内源性肾素和ACTH分泌均被阻断时,依他尼酸给药后PA升高幅度小得多。这种残余的升高主要可归因于依他尼酸给药前后所测定的醛固酮代谢清除率(MCR)的降低。所呈现的数据表明,急性容量耗竭后影响PA的多种因素可以被剖析出来,肾素、ACTH和MCR的降低各自都对PA的升高有作用。

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