[Leucostasis in the lung during hypovolemic-traumatic shock (author's transl)]

The cause of the posttraumatic respiratory distress syndrome is not yet well known and cannot be proved with certainty. The early stage of posttraumatic lung failure has been examined both from a morphological and biochemical aspect. Lung biopsies taken during hypovolemic-traumatic shock show besides endothelial damage an accumulation of leucocytes with free granules, similar to lysosomes. Based on these results further tests have been carried out to achieve a similar reaction in the hypovolemic-traumatic shock model in the dog, enabling us to undertake more extensive examinations and to use new methods of treatment. The lung biopsies taken at the beginning and after finishing the test were observed by light-transmission and scanning electron-microscope. Similar to the results obtained from humans, we found a massive leucostasis with degranulated cells. A parallel increase of lysosomal enzyme activity and a peripheral leucocytosis was seen while after reinfusion a distinct decrease was found. The massive occurence of leucocytes in the lung may be caused either by chemotaxis or by the sieve function of the lung after peripheral leucocytes aggregation. Both could have an immunological cause, especially due to involvement of the complement system. Septic reasons in the early stage of shock can be disregarded. More likely the complex effects of the interactions complement--fibrinolysis--kallikrein system are involved. Presumably the leucocytes caused direct damage to the endothelial cells. Lysosomal enzymes as reason for producing the damage would be one possibility; an other is the recently discovered effect of oxygen radicals produced during the close contact between leucocytes and endothelium and the simultaneously activated complement system.