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伴有正常细胞外液量的低氯性碱中毒

Chloride-depletion alkalosis with a normal extracellular fluid volume.

作者信息

Luke R G, Galla J H

出版信息

Am J Physiol. 1983 Oct;245(4):F419-24. doi: 10.1152/ajprenal.1983.245.4.F419.

DOI:10.1152/ajprenal.1983.245.4.F419
PMID:6312809
Abstract

Current concepts hold that volume expansion is essential to the correction of chloride-depletion alkalosis (CDA) with chloride repletion in a permissive role. In this scheme, intranephronal fluid reabsorption would be redistributed with increased delivery to the distal nephron where the provided chloride is readily reabsorbed and the limited capacity for bicarbonate reabsorption would promote bicarbonate excretion and correction of CDA. In a model of CDA produced by peritoneal dialysis against 0.15 M NaHCO3, we have shown complete correction of CDA within 24 h without volume expansion by either oral isotonic sodium or chloride salts with 70 mM chloride and despite an obligatory bicarbonate load and negative sodium and potassium balance. During correction of CDA without volume expansion in rats by intravenous isotonic fluids containing 80 mM chloride, fractional fluid and chloride reabsorptions in the proximal convoluted tubule and in the loop segment of superficial nephrons were not different from controls but chloride reabsorption was enhanced in the collecting duct segment and probably within the distal convolution. Despite no differences in serial hematocrits, blood pressure, and measured plasma volume, kidney and nephron glomerular filtration rate (GFR) were reduced in CDA and returned to normal upon recovery 24 h later.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

目前的观点认为,扩容对于通过补充氯离子来纠正氯耗竭性碱中毒(CDA)至关重要,其中补充氯离子起辅助作用。按照这种机制,肾内液体重吸收会重新分布,增加向远端肾单位的输送,在远端肾单位,补充的氯离子很容易被重吸收,而碳酸氢根重吸收能力有限会促进碳酸氢根排泄,从而纠正CDA。在通过腹膜透析对抗0.15M碳酸氢钠产生的CDA模型中,我们发现,通过口服含70mM氯离子的等渗钠盐或氯盐,在没有扩容的情况下,24小时内CDA可完全纠正,尽管有 obligatory碳酸氢根负荷以及钠和钾的负平衡。在大鼠中,通过静脉输注含80mM氯离子的等渗液体在不扩容的情况下纠正CDA时,近曲小管和浅表肾单位髓袢段的液体和氯离子重吸收分数与对照组无差异,但集合管段以及可能在远曲小管内的氯离子重吸收增强。尽管连续血细胞比容、血压和测得的血浆容量没有差异,但CDA时肾和肾单位的肾小球滤过率(GFR)降低,24小时后恢复时恢复正常。(摘要截断于250字)

相似文献

1
Chloride-depletion alkalosis with a normal extracellular fluid volume.伴有正常细胞外液量的低氯性碱中毒
Am J Physiol. 1983 Oct;245(4):F419-24. doi: 10.1152/ajprenal.1983.245.4.F419.
2
Segmental chloride and fluid handling during correction of chloride-depletion alkalosis without volume expansion in the rat.大鼠在纠正无容量扩张的氯耗竭性碱中毒过程中的节段性氯和液体处理
J Clin Invest. 1984 Jan;73(1):96-106. doi: 10.1172/JCI111211.
3
Effects of chloride and extracellular fluid volume on bicarbonate reabsorption along the nephron in metabolic alkalosis in the rat. Reassessment of the classical hypothesis of the pathogenesis of metabolic alkalosis.氯和细胞外液量对大鼠代谢性碱中毒时肾单位各段重吸收碳酸氢盐的影响。对代谢性碱中毒发病机制经典假说的重新评估。
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4
Volume-independent reductions in glomerular filtration rate in acute chloride-depletion alkalosis in the rat. Evidence for mediation by tubuloglomerular feedback.大鼠急性氯耗竭性碱中毒时肾小球滤过率的容量非依赖性降低。管球反馈介导的证据。
J Clin Invest. 1984 Dec;74(6):2002-8. doi: 10.1172/JCI111622.
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Volume expansion modulates NaHCO3 and NaCl transport in the proximal tubule and Henle's loop.容量扩张调节近端小管和髓袢中碳酸氢钠和氯化钠的转运。
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Bicarbonate transport in collecting duct segments during chloride-depletion alkalosis.氯耗竭性碱中毒时集合管各节段的碳酸氢盐转运
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Adaptations to chloride-depletion alkalosis.对氯缺乏性碱中毒的适应性变化。
Am J Physiol. 1991 Oct;261(4 Pt 2):R771-81. doi: 10.1152/ajpregu.1991.261.4.R771.

引用本文的文献

1
Renal bicarbonate reabsorption in the rat. II. Distal tubule load dependence and effect of hypokalemia.大鼠肾脏对碳酸氢盐的重吸收。II. 远端小管负荷依赖性及低钾血症的影响。
J Clin Invest. 1987 Aug;80(2):409-14. doi: 10.1172/JCI113087.
2
Effects of chloride and extracellular fluid volume on bicarbonate reabsorption along the nephron in metabolic alkalosis in the rat. Reassessment of the classical hypothesis of the pathogenesis of metabolic alkalosis.氯和细胞外液量对大鼠代谢性碱中毒时肾单位各段重吸收碳酸氢盐的影响。对代谢性碱中毒发病机制经典假说的重新评估。
J Clin Invest. 1987 Jul;80(1):41-50. doi: 10.1172/JCI113061.
3
New roles for chloride in renal physiology and pathophysiology.
氯离子在肾脏生理和病理生理中的新作用。
Trans Am Clin Climatol Assoc. 1991;102:84-93; discussion 93-5.