Progress in therapy has virtually eliminated death from primary shock and early infection following burns, but late mortality of patients from extensive burns has not been diminished. One of the lethal sequelae observed in patients with severe skin burns is lung damage. However, the pathophysiologic mechanism responsible for this sequela is not clearly elucidated. The purpose of this study is to investigate the ultrastructural changes of the lung injury and its mechanism in severly burned experimental animals.
Experimental animals were divided into 5 groups;groupⅠ, 5 Sprague-Dawley rats served as a control’groupⅡ,20 rats subjected to burns and sacrificed 1,3,5 and 7 days postburn intervals;groupⅢ,5 rats injured by burns and teated with dimethyl sulfoxide(DMSO), 1.5ml/kg administered intraperitoneally for 5 days, sacrifeced 5 days postburn;groupⅣ,5 rats injured by burns and treated with gabexate mesilate,50 mg/kg administered intraperitoneally for 5 days, sacrificed 5 days postburn;groupⅤ 5 rats subjucted to burns and treated with both DMSO and gabexate mesilate. The lungs of experimental animals were examined by electron imcroscopy. In order to observe the changes of alveolar capillary permeability in each group, vascular clearance test was performed with horseradish peroxidase(HRP).
The results were as follows;
Although minimal changes of the lungs began to appear from the 3rd day postburn, marked changes, such as alveolar capillary endothelial swelling, neutrophil and platelet infiltration, mitochondrial swelling of typeⅡ pneumocytes, along with interstitial edema were observed from the 5th day postburn. These changes were apparently alleviated in experimental groups treated with DMSO, gabexate mesilate, and DMSO plus gabexate mesilate.
Alveolar capillary permeability was markedly incresed from the 5th day postburn,demonstrated by leakage of HRP into the interstitium,which was diministhed in the experimental groups treated with DMSO,gabexate mesilate,and DMSO plus gabexate mesilate.
These findings suggest that the ultrastructural changes of the lungs induced by severe skin burns are significantly improved by absorption of hydroxyl radicals and by blocking of complement activation. It can be concluded that lung injury after severe skin burns is induced by activation of humoral mediator system.
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