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The acute respiratory distress syndrome (ARDS) is a severe inflammatory condition of the lung, which can be triggered by a number of different pulmonary and extra-pulmonary insults [1]. The characteristic pathological changes of ARDS include an exudative phase, with the accumulation of fluid within the lung, the release of pro-inflammatory cytokines and infiltration of inflammatory cells, especially neutrophils, into the lung parenchyma. Damage to the alveolar epithelium and pulmonary capillary endothelium occur and patients develop the characteristic histological appearance of diffuse alveolar damage [1]. This manifests clinically as non-cardiogenic pulmonary edema, which reduces lung compliance and impairs gas exchange.

The rise and fall of β-agonists in the treatment of ARDS