The objectives continue to be: 1) to understand the mechanisms of the inflammation leading to the lung injury of ARDS; 2) to understand the response of the acutely injured lungs to changes in physiological variables; and 3) to understand the epidemiology of ARDS in terms of prediction of ARDS occurence in course. All of these objectives are necessary steps in achieving the long-term goal of this SCOR, to design and test interventions which prevent or ameliorate the acute lung injury or limit its physiological effects. Specific studies and methodology include the following: 1) investigation of the role of leukotrienes, especially LTB4, in neutrophil chemotaxis in lung injury and of the production of lipoxygenase products of arachidonic acid (AA) by human endothelial cells; 2) investigation of the role of hydrogen peroxide and other toxic oxygen radicals produced by white blood cells in lung injury in endotoxemia and bone marrow infusion in animal models and interaction with AA metabolism; 3) study of acute effects of decreased pulmonary arterial blood flow in initial stages of lung injury and of the effect of reperfusion of an injured lobe after a period of no pulmonary blood flow; 4) study of mediators (especially AA metabolites) of the rise in bronchial blood flow following lung injury and measurements of regional bronchial blood flow with labeled microspheres; 5) study of extracellular matrix components in lung injury in humans and animal models by immunofluorescent techniques; 6) attempts to isolate cells, particularly alveolar Type II pneumocytes, from human lungs; 7) continued epidemiological study of patients at risk for ARDS; 8) study of the role of mediators in patients at risk for ARDS; and 9) studies of bronchoalveolar lavage in patients with ARDS emphasizing cellular dysfunction, mediators of injury, and fibroblast stimulation by BAL supernatant.
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