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[呼吸窘迫。肺水肿治疗的新视角]

[Respiratory distress. New Perspectives to lung edema treatment].

作者信息

Jaitovich A Ariel, Bertorello Alejandro M

机构信息

Departament of Molecular Medicine, Karolinska Hospital, Stockholm, Sweden.

出版信息

Medicina (B Aires). 2002;62(2):181-8.

Abstract

Acute respiratory distress syndrome (ARDS) is a life threatening condition associated with great morbidity and mortality. it is characterized initially by accumulation of fluid in the alveolar space that impairs alveolar oxygen exchange. Eventually, this syndrome leads to multiorgan failure. Therefore, rapid edema clearance has generally been associated with better outcome in patients with acute respiratory distress syndrome. Clearance of alveolar fluid is driven predominantly by active Na+ transport out of the alveolar space, mediated by increased apical Na(+)-channel and Na-K-ATPase activity. It has been demonstrated that increases in Na-K-ATPase in response to catecholamines in the alveolar epithelium are associated with increased lung edema clearance. The cellular mechanisms involve the recruitment of new Na-K-ATPase molecules to the plasma membrane from intracellular organelles. It also appears that adenovirus-mediated Na-K-ATPase gene transfer and increased Na-K-ATPase expression may provide an alternative and efficient pathway for transient increase in alveolar fluid reabsorption and resolution of pulmonary edema.

摘要

急性呼吸窘迫综合征(ARDS)是一种危及生命的疾病,具有很高的发病率和死亡率。其最初特征是肺泡腔内积液,这会损害肺泡的氧气交换。最终,该综合征会导致多器官功能衰竭。因此,快速清除水肿通常与急性呼吸窘迫综合征患者的更好预后相关。肺泡液的清除主要由主动的Na⁺转运出肺泡腔驱动,这由顶端Na⁺通道和Na-K-ATP酶活性增加介导。已经证明,肺泡上皮中儿茶酚胺引起的Na-K-ATP酶增加与肺水肿清除增加有关。细胞机制涉及从细胞内细胞器将新的Na-K-ATP酶分子募集到质膜。似乎腺病毒介导的Na-K-ATP酶基因转移和Na-K-ATP酶表达增加可能为肺泡液重吸收的短暂增加和肺水肿的消退提供一种替代且有效的途径。

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