Bench-to-bedside review: β2-Agonists and the acute respiratory distress syndrome
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* Corresponding author: Fang Gao f.g.smith@bham.ac.uk
1 Research Fellow, Intensive Care Unit, Birmingham Heartlands Hospital, Birmingham, UK
2 Specialist Registrar, Intensive Care Unit, Birmingham Heartlands Hospital, Birmingham, UK
3 Research Fellow, Lung Inflammation and Fibrosis Treatment Programme, Division of Medical Science, University of Birmingham, Birmingham, UK
4 Senior Lecturer, Lung Inflammation and Fibrosis Treatment Programme, Division of Medical Science, University of Birmingham, Birmingham, UK
5 Consultant, Intensive Care Unit, Birmingham Heartlands Hospital, Birmingham, UK
Critical Care 2004, 8:25-32 doi:10.1186/cc2417
Published: 23 December 2003Abstract
The acute respiratory distress syndrome (ARDS) is a devastating constellation of clinical, radiological and pathological signs characterized by failure of gas exchange and refractory hypoxia. Despite nearly 30 years of research, no specific pharmacological therapy has yet proven to be efficacious in manipulating the pathophysiological processes that underlie this condition. Several in vitro and in vivo animal or human studies suggest a potential role for β2-agonists in the treatment of ARDS. These agents have been shown to reduce pulmonary neutrophil sequestration and activation, accelerate alveolar fluid clearance, enhance surfactant secretion, and modulate the inflammatory and coagulation cascades. They are also used widely in clinical practice and are well tolerated in critically ill patients. The present review examines the evidence supporting a role for β2-agonists as a specific pharmacological intervention in patients with ARDS.