Alveolar epithelial fluid transport: basic mechanisms and clinical relevance.

M A Matthay, H R Flori, E R Conner, L B Ware
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Abstract

New evidence indicates that alveolar fluid clearance is driven by active sodium transport across the alveolar epithelium. Several in vivo as well as some in vitro studies indicate that vectorial sodium transport drives fluid clearance across the alveolar epithelium. This transport process can be upregulated by both catecholamine-dependent and catecholamine-independent mechanisms. Water transport appears to move across the alveolar epithelium primarily via transcellular water channels, recently termed aquaporins. Under some conditions, net alveolar fluid clearance continues even in the presence of acute lung injury. It is now possible to study the rate and mechanisms of alveolar fluid clearance in patients with either hydrostatic or increased permeability pulmonary edema. In addition, it may be possible to increase the rate of alveolar fluid clearance and hence the resolution of pulmonary edema in some patients, using aerosolized beta-adrenergic agonist therapy.

肺泡上皮液体运输:基本机制和临床相关性。
新的证据表明,肺泡液清除是由活跃的钠转运通过肺泡上皮驱动的。一些体内和一些体外研究表明,钠载体运输驱动肺泡上皮的液体清除。这种转运过程可以通过儿茶酚胺依赖性和儿茶酚胺非依赖性机制上调。水运输似乎主要通过跨细胞水通道在肺泡上皮中移动,最近被称为水通道蛋白。在某些情况下,即使存在急性肺损伤,净肺泡液清除仍在继续。现在有可能研究流体静力性或渗透性增加肺水肿患者肺泡液清除的速率和机制。此外,使用雾化的-肾上腺素能激动剂治疗可能会增加肺泡液清除率,从而缓解某些患者的肺水肿。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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