这是氯耗竭性碱中毒，而不是浓缩性碱中毒。
It is chloride depletion alkalosis, not contraction alkalosis.
机构信息
Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
出版信息
J Am Soc Nephrol. 2012 Feb;23(2):204-7. doi: 10.1681/ASN.2011070720. Epub 2012 Jan 5.
Abstract
Maintenance of metabolic alkalosis generated by chloride depletion is often attributed to volume contraction. In balance and clearance studies in rats and humans, we showed that chloride repletion in the face of persisting alkali loading, volume contraction, and potassium and sodium depletion completely corrects alkalosis by a renal mechanism. Nephron segment studies strongly suggest the corrective response is orchestrated in the collecting duct, which has several transporters integral to acid-base regulation, the most important of which is pendrin, a luminal Cl/HCO(3)(-) exchanger. Chloride depletion alkalosis should replace the notion of contraction alkalosis.
摘要
代谢性碱中毒的维持通常归因于氯缺失引起的容量收缩。在大鼠和人类的平衡和清除研究中，我们表明，在持续碱负荷、容量收缩以及钾和钠耗竭的情况下补充氯，通过肾脏机制完全纠正碱中毒。肾单位节段研究强烈表明，纠正反应是在集合管中协调的，集合管中有几个对酸碱调节至关重要的转运体，其中最重要的是顶端膜的 Cl/HCO3- 交换体 pendrin。氯缺失性碱中毒应该取代收缩性碱中毒的概念。
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