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Published online by Cambridge University Press: 17 February 2017
In discussions of the pathogenesis of posttraumatic respiratory distress syndrome (adult respiratory distress syndrome, ARDS), thromboembolism or microembolism (6) is the most frequently suggested mechanism. Embolic material released from the site of injury and/or intravascularly formed aggregates of platelets and fibrin are thought to plug the pulmonary capillaries, giving rise to diffuse pulmonary damage. Pulmonary trapping of platelets and fibrin has been studied in various animal models in which intravascular aggregation was induced pharmacologically, without trauma (2). Studies in patients with ARDS are difficult to standardize, and the results therefore are often inconclusive. We have evolved an experimental model (5) by means of which changes identical to ARDS can be induced from reproducible musculoskeletal trauma in anesthetized pigs. The pigs are observed under anesthesia for three days after the trauma under standardized and carefully controlled conditions. The aim of the present study was to use this model for registration and monitoring of pulmonary trapping of platelets and fibrin in animals with ARDS following standardized trauma, without adding any pharmacologic substance that could influence platelet aggregation or fibrinolysis. Pulmonary trapping was determined by external detection of 51Cr-labeled homologous platelets and 125I-labeled human fibrinogen, intravenously administered before anesthesia and trauma.