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饮食中的氯化钠决定了钾缺乏诱导的代谢性碱中毒的严重程度。

Dietary NaCl determines severity of potassium depletion-induced metabolic alkalosis.

作者信息

Hernandez R E, Schambelan M, Cogan M G, Colman J, Morris R C, Sebastian A

出版信息

Kidney Int. 1987 Jun;31(6):1356-67. doi: 10.1038/ki.1987.150.

Abstract

It is uncertain whether, in humans, potassium depletion can cause or sustain metabolic alkalosis of clinically important degree in the absence of coexisting known alkalosis-producing conditions. Previously we found, in normal humans ingesting abundant NaCl, that dietary K+ depletion alone can induce and sustain a small decrease in blood acidity and increase in plasma bicarbonate concentration; we hypothesized that more severe alkalosis was prevented by mitigating mechanisms initiated by renal retention of dietary NaCl that was induced by K+ depletion. To ascertain the acid-base response to dietary K+ depletion under conditions in which the availability of NaCl for retention is greatly limited, in the present study of six normal men we restricted dietary K+ as in the previous study except that intake of NaCl was maintained low (2 to 7 mEq/day, Low NaCl Group) instead of high (126 mEq/day, High NaCl Group). Plasma acid-base composition and renal net-acid excretion (NAE) did not differ significantly between groups during the control period. In the steady state of K+ depletion (days 11 to 15 of K+ restriction), neither plasma K+ concentration (2.9 +/- 0.9 mEq/liter vs. 3.0 +/- 0.1 mEq/liter) nor cumulative K+ deficit (399 +/- 59 mEq vs. 466 +/- 48 mEq) differed significantly between groups. During K+ restriction, persisting metabolic alkalosis developed in both groups, which was more severe in the Low NaCl Group: increment in [HCO3-]p, 7.5 +/- 1.0 mEq/liter versus 2.0 +/- 0.3 mEq/liter, P less than 0.001; decrement in [H+]p, 5.5 +/- 0.6 nEq/liter versus 2.9 +/- 0.4 nEq/liter, P less than 0.003. A significantly more severe alkalosis in the Low NaCl Group was evident at all degrees of K+ deficiency achieved during the course of the 15 days of K+ restriction, and the severity of alkalosis in the Low NaCl Group correlated with the degree of K+ deficiency. During the generation of alkalosis (days 1 to 7 of K+ restriction), NAE increased in the Low NaCl Group whereas it decreased in the High NaCl Group. During the maintenance of alkalosis (days 11 to 15), NAE stabilized in both groups after it returned to values approximating the control values. In both groups, urine Cl- excretion decreased during K+ restriction even though Cl- intake had not been changed, with the result that body Cl- content increased negligibly in the Low NaCl Group (28 +/- 6 mEq) and substantially in the High NaCl Group (355 +/- 64 mEq).(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

在没有已知并存的产碱条件下,钾缺乏在人类中是否会导致或维持具有临床重要程度的代谢性碱中毒尚不确定。此前我们发现,在摄入大量氯化钠的正常人体内,仅饮食中钾缺乏就能诱导并维持血液酸度的小幅降低和血浆碳酸氢盐浓度的升高;我们推测,更严重的碱中毒是由钾缺乏诱导的肾脏对饮食中氯化钠的潴留所引发的缓解机制所预防的。为了确定在氯化钠潴留的可用性受到极大限制的条件下,饮食中钾缺乏时的酸碱反应,在本研究中,我们对6名正常男性进行了研究,与之前的研究一样限制饮食中的钾,但氯化钠摄入量维持在低水平(2至7 mEq/天,低氯化钠组),而不是高水平(126 mEq/天,高氯化钠组)。在对照期内,两组之间的血浆酸碱组成和肾脏净酸排泄(NAE)没有显著差异。在钾缺乏的稳定期(钾限制的第11至15天),两组之间的血浆钾浓度(2.9±0.9 mEq/升对3.0±0.1 mEq/升)和累积钾缺乏量(399±59 mEq对466±48 mEq)均无显著差异。在钾限制期间,两组均出现了持续的代谢性碱中毒,低氯化钠组更为严重:[HCO3-]p的增加,7.5±1.0 mEq/升对2.0±0.3 mEq/升,P<0.001;[H+]p的降低,5.5±0.6 nEq/升对2.9±0.4 nEq/升,P<0.003。在钾限制的15天过程中,在所有达到的钾缺乏程度下,低氯化钠组的碱中毒明显更严重,且低氯化钠组碱中毒的严重程度与钾缺乏程度相关。在碱中毒的产生期(钾限制的第1至7天),低氯化钠组的NAE增加,而高氯化钠组的NAE降低。在碱中毒的维持期(第11至15天),两组的NAE在恢复到接近对照值后均趋于稳定。在两组中,尽管氯摄入量未改变,但在钾限制期间尿氯排泄减少,结果低氯化钠组的体内氯含量略有增加(28±6 mEq),而高氯化钠组的体内氯含量大幅增加(355±64 mEq)。(摘要截断于400字)

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