Despite improvements in general supportive care and ventilatory strategies designed to limit lung injury, no specific pharmacological therapy has yet proven to be efficacious in the management of acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS). Based on experimental studies, as well as studies of the ex-vivo human lung, pulmonary edema fluid clearance from the alveolar space can be augmented by both inhaled and systemic beta2-adrenoceptor agonists (beta2-agonists). Additionally, in the presence of lung injury, beta2-agonists may reduce lung vascular permeability. Treatment with beta2-agonists may also increase the secretion of surfactant and have anti-inflammatory effects. In view of these potentially beneficial effects, beta2-agonist therapy should be evaluated for the treatment of lung injury in humans, particularly because they are already in wide clinical use and do not seem to have serious adverse effects in critically ill patients.