Mechanisms of pulmonary edema clearance during acute hypoxemic respiratory failure: Role of the Na,K-ATPase

Mechanisms of pulmonary edema clearance during acute hypoxemic respiratory failure: Role of the Na,K-ATPase
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DOI:
10.1097/01.ccm.0000057895.22008.ec
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发表时间:
2003-04-01
影响因子:
8.8
通讯作者:
Sznajder, JI
Sznajder, JI
中科院分区:
医学1区
文献类型:
--
作者:
Dada, LA;Sznajder, JI

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肺水肿是急性呼吸窘迫综合征的标志。当肺泡毛细血管屏障的渗透性增加,导致肺泡充盈和气体交换受损时,就会发生这种情况。肺泡液吸收的机制与肺泡水肿形成的机制不同。肺泡液吸收。进入血管主要是通过水沿着渗透梯度主动将钠离子 (Na+) 从肺泡腔中转运出来。 Na+ 穿过肺泡上皮的转运以及肺泡液的吸收受顶端 Na+ 通道、基底外侧钠钾-腺苷三磷酸酶 (Na,K-ATPase) 以及可能的氯离子通道的调节。 Na,K-ATP 酶已定位于肺泡上皮,其在促进肺水肿清除方面的重要性已得到证实。在肺损伤模型中,一些报告表明,异丙肾上腺素和多巴胺等儿茶酚胺上调 Na+ 通道和 Na,K-ATP 酶,导致肺泡液吸收增加。尽管重组基因技术还不是治疗肺水肿的治疗选择,但一些实验研究报告称,Na,K-ATP酶基因的过度表达会导致高氧性肺损伤期间液体吸收增加。有重要证据表明肺损伤患者的液体清除能力受到损害。旨在提高肺泡上皮吸收水肿能力的治疗策略应该会给急性呼吸窘迫综合征患者带来好处。
Pulmonary edema is the hallmark of acute respiratory distress syndrome. It occurs when the permeability of the alveolar-capillary barrier is increased, causing alveolar flooding and impaired gas exchange. The mechanisms of alveolar fluid resorption are different from those of alveolar edema formation. Alveolar fluid resorption. into the vessels is brought about mainly by active transport of sodium ions (Na+) out of the alveolar spaces with water following the osmotic gradient. Na+ transport across the alveolar epithelium, and thus alveolar fluid resorption, is regulated by apical Na+ channels, the basolateral sodium potassium-adenosine triphosphatase (Na,K-ATPase), and possibly chloride channels. The Na,K-ATPase has been localized to the alveolar epithelium and the importance of its role in contributing to lung edema clearance has been demonstrated. In models of lung injury, several reports have shown that catecholamines such as isoproterenol and dopamine up-regulate Na+ channels and the Na,K-ATPase giving rise to increased alveolar fluid resorption. Although recombinant gene technology is not yet a therapeutic option for the treatment of pulmonary edema, several experimental studies have reported that overexpression of Na,K-ATPase genes causes increased fluid resorption during hyperoxic lung injury. There is significant evidence that fluid clearance is impaired in patients with lung injury. Therapeutic strategies aimed at increasing the ability of alveolar epithelium to resorb the edema should lead to benefits for patients with acute respiratory distress syndrome.