VEGF is predominantly expressed by alveolar type II cells in the lung,21 with contributions from macrophages and neutrophils during inflammatory responses.22 In this context, the role of VEGF in the lung is as a potent stimulus for endothelial and epithelial repair.23, 24 The decrease in VEGF observed from 96 h in this model closely resembles the reduced VEGF levels observed in patients with ALI, which may be associated with impaired repair responses or reflect specific loss of alveolar type II cells following injury.25 Decline in lung function was also maximal at 96 h. This evidence concerns the gene VEGFA and acute respiratory distress syndrome.