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β受体刺激诱导急性肺损伤和肺水肿改善的机制。

Mechanisms of beta-receptor stimulation-induced improvement of acute lung injury and pulmonary edema.

作者信息

Groshaus Horacio E, Manocha Sanjay, Walley Keith R, Russell James A

机构信息

Critical Care Research Laboratories, St Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada.

出版信息

Crit Care. 2004 Aug;8(4):234-42. doi: 10.1186/cc2875. Epub 2004 May 25.

Abstract

Acute lung injury (ALI) and the acute respiratory distress syndrome are complex syndromes because both inflammatory and coagulation cascades cause lung injury. Transport of salt and water, repair and remodeling of the lung, apoptosis, and necrosis are additional important mechanisms of injury. Alveolar edema is cleared by active transport of salt and water from the alveoli into the lung interstitium by complex cellular mechanisms. Beta-2 agonists act on the cellular mechanisms of pulmonary edema clearance as well as other pathways relevant to repair in ALI. Numerous studies suggest that the beneficial effects of beta-2 agonists in ALI include at least enhanced fluid clearance from the alveolar space, anti-inflammatory actions, and bronchodilation. The purposes of the present review are to consider the effects of beta agonists on three mechanisms of improvement of lung injury: edema clearance, anti-inflammatory effects, and bronchodilation. This update reviews specifically the evidence on the effects of beta-2 agonists in human ALI and in models of ALI. The available evidence suggests that beta-2 agonists may be efficacious therapy in ALI. Further randomized controlled trials of beta agonists in pulmonary edema and in acute lung injury are necessary.

摘要

急性肺损伤(ALI)和急性呼吸窘迫综合征是复杂的综合征,因为炎症和凝血级联反应都会导致肺损伤。盐和水的转运、肺的修复和重塑、细胞凋亡以及坏死是其他重要的损伤机制。肺泡水肿通过复杂的细胞机制将盐和水从肺泡活跃转运至肺间质而得以清除。β2激动剂作用于肺水肿清除的细胞机制以及ALI中与修复相关的其他途径。大量研究表明,β2激动剂在ALI中的有益作用至少包括增强肺泡腔液体清除、抗炎作用和支气管扩张。本综述的目的是探讨β激动剂对改善肺损伤的三种机制的影响:水肿清除、抗炎作用和支气管扩张。本更新内容特别回顾了β2激动剂在人类ALI及ALI模型中作用的证据。现有证据表明,β2激动剂可能是ALI的有效治疗方法。有必要进一步开展β激动剂治疗肺水肿和急性肺损伤的随机对照试验。

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本文引用的文献

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Long-term stimulation of alveolar epithelial cells by beta-adrenergic agonists: increased Na+ transport and modulation of cell growth?
Am J Physiol Lung Cell Mol Physiol. 2003 Oct;285(4):L798-801. doi: 10.1152/ajplung.00166.2003.
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Postreceptor defects in alveolar epithelial beta-adrenergic signaling after prolonged isoproterenol infusion.
Am J Physiol Lung Cell Mol Physiol. 2003 Sep;285(3):L578-83. doi: 10.1152/ajplung.00339.2002. Epub 2003 May 16.
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Chloride and potassium channel function in alveolar epithelial cells.肺泡上皮细胞中氯离子和钾离子通道的功能
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