• Guo-dong Huo, Shao-xi Cai, Ying-hua Chen, and Bo Chen.
• Department of Respiratory Diseases, Nanfang Hospital, and Department of Histology and Embryology, Southern Medical University, Guangzhou 510515, China. hgd77223@fimmu.com
• Nan Fang Yi Ke Da Xue Xue Bao. 2007 Jul 1;27(7):998-1002.

ObjectiveTo investigate the effects of inflammatory mediators in the serum of rats with ventilator-induced lung injury (VILI) on endothelial cellular cytoskeleton and monolayer cellular permeability and explore the molecular mechanism of VILI-induced lung edema.MethodsThirty healthy male SD rats were divided into 3 groups, namely group A with normal tidal volume ventilation, group B with high tidal volume ventilation and group C with high tidal volume ventilation plus ulinastatin treatment. The serum was collected from each rat after ventilation and added into endothelial cell line ECV-304 culture medium, and 2 h later the changes of F-actin and cell permeability were observed.ResultsCompared to sera from rats with normal tidal volume ventilation, the sera of rats with high tidal volume ventilation caused obvious reorganization of actin cytoskeleton with weakened fluorescent intensity at the peripheral filament bands and formation of long and thick stress fibers in the center, which resulted in endothelial contraction and increased cell permeability. Pretreatment with ulinastatin could lessen these changes significantly. The percentage in change of permeability coefficient (Ppa%) after stimulation with the sera of rats in groups A, B and C was (6.95+/-1.66)%, (27.50+/-7.77)%, and (17.71+/-4.66)%, respectively, showing statistically significant differences (P<0.05).ConclusionThe pro-inflammatory mediators in the serum of rats with high tidal volume ventilation increases endothelial cell permeability by reorganizing actin cytoskeleton, and pretreatment with ulinastatin can lessen the hyperpermeability by inhibiting multiple pro-inflammatory mediators.

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