Exogenous surfactant protects against endotoxin induced acute respiratory distress syndrome in rodents via vascular endothelial growth factor.

Vascular endothelial growth factor (VEGF) is a potent angiogenic factor which is abundantly expressed in the normal lung and is released by numerous cell types. Using a bacteria-induced lung injury model and surfactant therapy in rats, VEGF expression in lung was investigated. Sprague Dawley male rats were divided into four groups: buffer controls; rats challenged with LPS (055:B5 E. coli); challenged with LPS and treated with porcine surfactant (P-SF); and challenged with LPS and treated with synthetic surfactant (S-SF). The expressions of VEGF, PCNA, and BrdU were studied. VEGF protein expression was decreased in comparison to the control rats, as seen by both Western immunoblot and immunohistochemistry. Protein expression of PCNA and proliferation index as determined by both PCNA and BrdU immunostaining were also seen to be decreased in the LPS-treated animals, and with the surfactant treatment the expression was increased. The downregulation of VEGF in the alveolar space may reflect the recovery from acute lung injury, which leads to the limited endothelial permeability, and may participate in the decrease in capillary number, as observed during acute respiratory distress syndrome with potentially significant clinical consequences.