Translational research : the journal of laboratory and clinical medicine
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Disruption of epithelial and endothelial barriers found in patients with acute lung injury often results in the need for the support of mechanical ventilation. High tidal volume (V(T)) mechanical ventilation can increase lung damage through lung inflammation, but the mechanisms are unclear. We hypothesized that a colloid supply with hydroxyethyl starch would decrease neutrophil infiltration, lung edema, and vascular endothelial growth factor (VEGF) production in mice exposed to high V(T) mechanical ventilation. ⋯ High V(T) ventilation induced the increases of microvascular permeability, neutrophil influx, expressions of VEGF mRNA and VEGF, production of VEGF protein, positive staining of VEGF in epithelium, and apoptotic epithelial cell death. Lung injury induced by high V(T) ventilation was attenuated with the supply of hydroxyethyl starch and pharmacologic inhibition of VEGF expression by siRNA. We conclude that hydroxyethyl starch reduces high V(T) mechanical ventilation-induced lung injury and neutrophil infiltration through an inhibition of VEGF expression.