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慢性肾衰竭患者经细胞钾分泌增强的机制

Mechanism of enhanced transcellular potassium-secretion in man with chronic renal failure.

作者信息

Panese S, Mártin R S, Virginillo M, Litardo M, Siga E, Arrizurieta E, Hayslett J P

出版信息

Kidney Int. 1987 Jun;31(6):1377-82. doi: 10.1038/ki.1987.152.

Abstract

Previous studies from our laboratory demonstrated that net K secretion in human rectum was 2.5-fold higher in patients with chronic renal failure than in controls. The present study was performed to determine whether K secretion in human large intestine involves an active process and whether an active transport process accounts, at least in part, for the rise in net K secretion in patients with renal insufficiency. Studies were performed under conditions when net water and electrolyte transport approached zero, and the observed distribution of K and Na across the rectal mucosa was compared to expected equilibrium values. In control subjects an active transport of 27.6 +/- 2.6 mV was observed for K and 63 +/- 4.2 mV for Na. Similar values were demonstrated in patients with chronic renal failure. The results of these studies demonstrated that net secretion of K and absorption of Na are governed, at least in part, by active transport processes, and suggest that, since active K secretion is not impaired, the rise in net K secretion in patients with renal insufficiency is caused by active secretion as well as by passive driving forces.

摘要

我们实验室之前的研究表明,慢性肾衰竭患者直肠的钾净分泌量比对照组高2.5倍。本研究旨在确定人类大肠中的钾分泌是否涉及一个主动过程,以及主动转运过程是否至少部分地解释了肾功能不全患者钾净分泌量的增加。研究在净水和电解质转运接近零的条件下进行,并将直肠黏膜上钾和钠的观察分布与预期平衡值进行比较。在对照组中,观察到钾的主动转运为27.6±2.6 mV,钠的主动转运为63±4.2 mV。慢性肾衰竭患者也得到了类似的值。这些研究结果表明,钾的净分泌和钠的吸收至少部分受主动转运过程的控制,并表明,由于主动钾分泌未受损,肾功能不全患者钾净分泌量的增加是由主动分泌以及被动驱动力引起的。

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