Early responses of VEGF during acute lung injury induced by seawater immersion after open chest trauma.

Background: Immersion in seawater after open chest trauma may induce acute lung injury. Higher osmotic pressure is one of the main characteristics of seawater. The effects of vascular endothelial growth factor (VEGF) on endothelial cell permeability and proliferation have been demonstrated in studies. The early responses and effects of the VEGF on acute lung injury induced by seawater immersion after open chest trauma (SWI-ALI) are unknown.

Objective: To investigate the levels of VEGF and its receptors in SWI-ALI and further explore whether the levels of VEGFs are connected with the pathogenesis of SWI-ALI.

Methods: We put dogs into group 'seawater' and group 'control'. The control group only suffered from open chest trauma, whereas the seawater group was exposed to seawater after trauma. The levels of total protein in plasma and bronchoalveolar lavage fluid were measured to calculate the pulmonary permeability index. 0, 2, 4, 6 and 8 h after open chest trauma, the plasma samples were collected to test the levels of VEGFs with ELISA kit. Western blotting and real-time RT-PCR were used to measure the VEGF levels in lung.

Results: Compared with control animals, plasma osmotic pressure, VEGF and sVEGFR-1 significantly increased in plasma, while VEGF and VEGFR-2 significantly increased in seawater-immersion lung tissue. The levels of VEGF in plasma were significantly correlated with plasma osmotic pressure and pulmonary permeability index.

Conclusion: Early release of VEGFs increases pulmonary vascular permeability and partially leads to the development of SWI-ALI. VEGFs may have a crucial role in the early onset of SWI-ALI.