Berthiaume Yves, Folkesson Hans G, Matthay Michael A
Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Université de Montréal, Montréal, Quebec, Canada H2W 1T7.
J Appl Physiol (1985). 2002 Dec;93(6):2207-13. doi: 10.1152/japplphysiol.01201.2001.
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.
肺水肿的消退涉及活跃的跨上皮钠转运。虽然其中一些相关的细胞和分子机制已得到较好理解，但直到最近才开始评估这些机制在损伤肺中的调控情况。有趣的是，在轻度至中度肺损伤中，肺泡水肿液清除通常得以保留。这种保留或增强的肺泡液清除是由儿茶酚胺依赖性或非依赖性机制介导的。这种对肺泡液清除的刺激与钠转运分子（如上皮钠通道或钠钾ATP酶泵）的激活或表达增加有关，并且可能还涉及囊性纤维化跨膜传导调节因子。当发生严重肺损伤时，肺泡液清除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变化有关。多种药理学手段，如β-肾上腺素能激动剂、血管活性药物或基因治疗，可能被证明在促进损伤肺中肺泡水肿的消退方面有效。
