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.
Highlights
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are important because of the continued high mortality and costs of care of these conditions
Beta adrenergic agonists are inexpensive and are often used in the treatment of patients who have ALI or ARDS for reasons not related to attempts to improve resolution of lung injury
Laffon and colleagues [16] showed that intravenous lidocaine, a sodium channel inhibitor, decreased baseline alveolar epithelial fluid clearance by 50% in rats when albumin solution was instilled into distal air spaces, and that this effect was reversed by terbutaline
Summary
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are important because of the continued high mortality and costs of care of these conditions. A common feature of ALI/ARDS, may in addition contribute to impaired edema clearance because hypoxia decreases expression of subunits of the sodium channel and of the Na,K-ATPase pump [24] These mechanisms are important in the role of beta-2 agonists in the clearance of alveolar edema. Laffon and colleagues [16] showed that intravenous lidocaine, a sodium channel inhibitor, decreased baseline alveolar epithelial fluid clearance by 50% in rats when albumin solution was instilled into distal air spaces, and that this effect was reversed by terbutaline This strongly suggested the importance of increased transport of sodium across the alveolar epithelium and of beta adrenergic receptor stimulation in stimulating alveolar fluid clearance. The beta agonists terbutaline and salmeterol increased phosphatidylcholine secretion by adult and fetal type II cells [60] in a dose-dependent manner
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