Abstract

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are associated with disruption of the alveolo-capillary barrier, which results in edema fluid accumulation and impaired gas exchange. Despite nearly 30 years of research,no specific pharmacological therapy has yet proven to be efficacious in manipulating the pathophysiological processes. Several in vitro and in vivo animal or human studies suggest a potential role for β2 agonists in the treatment of ALI/ARDS. Terbutaline has been shown to reduce pulmonary neutrophil sequestration and activation, decrease pulmonary microvascular permeability, accelerate alveolar fluid clearance, thus attenuating pulmonary edema and improving gas exchange. However, further work with large animals and patients is needed to confirm these findings and to determine the physiological benefits of the terbutaline effect and the doseresponse relationship. Key words: Terbutaline; Pulmonary edema; Acute lung inury

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