Lung edema clearance: 20 years of progress - Invited review: Alveolar edema fluid clearance in the injured lung
Lung edema clearance: 20 years of progress - Invited review: Alveolar edema fluid clearance in the injured lung
复制标题
DOI：
10.1152/japplphysiol.01201.2001
复制
发表时间：
2002-12-01
影响因子：
3.3
通讯作者：
Matthay, MA
中科院分区：
文献类型：
--
作者：
Berthiaume, Y;Folkesson, HG;Matthay, MA
肺水肿的消退涉及主动跨上皮钠转运。虽然几个涉及的细胞和分子机制是相对较好的理解，它只是最近，这些机制在受伤的肺正在评估的监管。有趣的是，在轻度至中度肺损伤中，肺泡水肿液体清除通常被保留。这种保留或增强的肺泡液体清除是由儿茶酚胺依赖性或非依赖性机制介导的。肺泡液体清除的这种刺激与钠转运分子如上皮钠通道或Na+-K+-ATP酶泵的激活或表达增加有关，也可能涉及囊性纤维化跨膜传导调节因子。当发生严重肺损伤时，肺泡液体清除率的降低可能与肺泡通透性的变化或钠或氯转运分子的活性或表达的变化有关。多种药理学工具，如β-肾上腺素能受体激动剂，血管活性药物，或基因治疗可能被证明是有效的，刺激在受损的肺肺泡水肿的决议。
Resolution of pulmonary edema involved active transepithelial sodium transport. Although several of the cellular and molecular mechanisms involved are relatively well understood, it is only recently that the regulation of these mechanisms in injured lung are being evaluated. Interestingly, in mild-to-moderate lung injury, alveolar edema fluid clearance is often preserved. This preserved or enhanced alveolar fluid clearance is mediated by catecholamine-dependent or -independent mechanisms. This stimulation of alveolar liquid clearance is related to activation or increased expression of sodium transport molecules such as the epithelial sodium channel or the Na+-K+-ATPase pump and may also involve the cystic fibrosis transmembrane conductance regulator. When severe lung injury occurs, the decrease in alveolar liquid clearance may be related to changes in alveolar permeability or to changes in activity or expression of sodium or chloride transport molecules. Multiple pharmacological tools such as beta-adrenergic agonists, vasoactive drugs, or gene therapy may prove effective in stimulating the resolution of alveolar edema in the injured lung.