We studied the changes of pulmonary vascular permeability andlipoperoxides in scalded rats with full-thickness damage 40％ of bow surface. Theresults showed that both pulmonary vascular permeability and lipoperoxides inserum and lung homogenate increased significantly 2 h after scalding.Subsequently,interstitial and alveolar edema developed.Pulmonary vascularpermeability was strongly correlated with lung lipoperoxides(r=0.992).SerumCH_(50)was decreased to 56.8％ 1 h after scalding,and at the same time,neutrophilcount increased in pulmonary interstitium and vasculature.The increase inpulmonary vascular permeability and lipoperoxides could be prevented with largedose of vitamin E and neutropenia.The results indicate that the lipoperoxidationof pulmonary vascular endothelial cells secondary to complement activation andpulmonary leukostasis is the major cause of increase in pulmonary vascularpermeability after scalding. We studied the changes of pulmonary vascular permeability and lipoperoxides in scalded rats with full-thickness damage 40% of bow surface. Theresults showed that both pulmonary vascular permeability and lipoperoxides inserum and lung homogenate increased significantly for 2 h after scalding. Published, interstitial and alveolar edema developed . Pulmonary vascular performance was significantly correlated with lung lipoperoxides (r = 0.992) .Serum CH_ (50) was decreased to 56.8% 1 h after scalding, and at the same time, neutrophil count increased in pulmonary interstitium and vasculature. The increase in pulmonary vascular permeability and lipoperoxides could be prevented with large dose of vitamin E and neutropenia. The results indicate that the lipoperoxidation of pulmonary vascular endothelial cells secondary to complement activation and pulmonary leukostasis is the major cause of increase in pulmonary vascular performance after scalding.