Acute lung injury is an important cause of respiratory failure in the critically ill patient. It is caused by damage to the alveolar barrier with subsequent alveolar flooding leading to the development of refractory hypoxaemia. Beta agonists stimulate alveolar fluid clearance in animal models of lung injury. In a clinical trial (BALTI-1) intravenous beta agonists reduced extravascular lung water – an effect that took 72 hours in contrast to what animal studies suggest. One possible explanation for the delay in change in extravascular lung water is the time required for salbutamol to stimulate alveolar epithelial repair. Objective: To investigate whether salbutamol can stimulate alveolar epithelial repair in-vivo and in-vitro. Findings: Intravenous salbutamol reduced measures of alveolar-capillary permeability in patients with ARDS. In vitro, salbutamol stimulated both wound repair, spreading and proliferation of A549 cells and distal lung epithelial cells. Lung lavage fluid from patients treated with salbutamol enhanced wound repair responses compared to placebo treated patients in vitro by an IL1-â dependent mechanism. Conclusions: Our in-vivo and in-vitro work suggests that salbutamol may stimulate epithelial repair – potentially a pharmacological first in ARDS. Clearly establishing the mechanisms and pathways responsible for this is important for the future, and may allow the identification of novel therapeutic targets to promote alveolar epithelial repair in humans with ARDS.
- acute lung injury
- beta agonist
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