Vadász István, Raviv Stacy, Sznajder Jacob I
Division of Pulmonary and Critical Care Medicine, Feinberg School of Medicine, Northwestern University, 240 E. Huron Street, McGaw 2300, 60611, Chicago, IL, USA.
Intensive Care Med. 2007 Jul;33(7):1243-1251. doi: 10.1007/s00134-007-0661-8. Epub 2007 May 25.
Active transport of sodium across the alveolar epithelium, undertaken in part by the Na,K-adenosine triphosphatase (Na,K-ATPase), is critical for clearance of pulmonary edema fluid and thus the outcome of patients with acute lung injury. Acute lung injury results in disruption of the alveolar epithelial barrier and leads to impaired clearance of edema fluid and altered Na,K-ATPase function. There has been significant progress in the understanding of mechanisms regulating alveolar edema clearance and signaling pathways modulating Na,K-ATPase function during lung injury. The accompanying review by Morty et al. focuses on intact organ and animal models as well as clinical studies assessing alveolar fluid reabsorption in alveolar epithelial injury. Elucidation of the mechanisms underlying regulation of active Na+ transport, as well as the pathways by which the Na,K-ATPase regulates epithelial barrier function and edema clearance, are of significance to identify interventional targets to improve outcomes of patients with acute lung injury.
钠通过肺泡上皮的主动转运,部分由钠钾三磷酸腺苷酶(Na,K - ATPase)承担,对肺水肿液的清除至关重要,因此对急性肺损伤患者的预后也很关键。急性肺损伤会导致肺泡上皮屏障破坏,进而导致水肿液清除受损以及钠钾三磷酸腺苷酶功能改变。在理解调节肺泡水肿清除的机制以及肺损伤期间调节钠钾三磷酸腺苷酶功能的信号通路方面已经取得了重大进展。Morty等人随后的综述重点关注完整器官和动物模型以及评估肺泡上皮损伤中肺泡液体重吸收的临床研究。阐明主动钠转运调节的潜在机制,以及钠钾三磷酸腺苷酶调节上皮屏障功能和水肿清除的途径,对于确定改善急性肺损伤患者预后的干预靶点具有重要意义。