Objective    To study the mechanism of acute lung injury secondary to isolated severe head injury.     Methods    Twenty-two male SD rats were randomly divided into normal group (NG

n=4)

and trauma group (TG

n=18) which were sacrificed respectively on day 1

3

7. The pathomorphological changes were observed by light and electron microscope. The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-8 (IL-8) in bronchoalveolar lavage fluid (BALF) were investigated by radioassay (RIA). The level of soluble intercellular adhesion molecule-1(sICAM-1) in BALF was measured by enzyme linked immunosorbent assay (ELISA).     Results    Capillary congestion

inflammatory cell infiltration and thickening of alveolar septum were detected in TG from day 1 to 7 by light microscope. The histological score of lung on day 3 in TG was significantly higher than that on day 1 and 7. The ultramicroscopic structure of lung showed swelling of vascular endothelial cells

infiltration of polymorphonuclear neutrophil and monocyte

injury of pulmonary epithelial cells in TG from day 1 to 7. The levels of TNF-α

IL-8 and sICAM-1 in BALF in TG were significantly higher than that in NG and the peak values were on day 3. The histologic score in TG was positively correlated with the levels of TNF-α

IL-8 and sICAM-1 in BALF.     Conclusion    Isolated severe head injury could induce acute lung injury that reached the most severe degree on day 3. The elevation of such proinflammatory cytokines as TNF-α

IL-8 and sICAM-1 in BALF plays an important role in the development of excessive inflammatory response of lung injury secondary to isolated severe head injury.