Mechanism of acute lung injury secondary to isolated severe head injury in rats

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.