Pulmonary microembolism results in lung vascular injury characterized by an increase in the transport of the pulmonary micro- vascular barrier into proteins. The increase in lung vascular permeability is a primary factor responsible for the protein-rich oedema associated with pulmonary microembolism. The microembolism can result from a variety of causes, but an essential feature of it is the "plugging" of pulmonary microvessels with thrombi; that is, the entrapment of fibrin and blood-formed elements in pulmonary microvessels. Neutrophil-derived products released subsequent to neutrophil activation are primary mediators of lung vascular injury. The attachment of neutrophils to the endothelial cell is a requisite for the development of endothelial injury. Fibrin itself plays another important role in that fibrin promotes neutrophil adhesiveness and releases factors such as fibrin degradation products which may increase endothelial permeability. Therefore, pulmonary microembolism is a determinant of acute lung microvascular injury and is a factor in the pathogenesis of the adult respiratory distress syndrome. Neutrophils are important effector cells mediating lung microvascular injury, although the factors that are responsible for neutrophil sequestration and activation remain unclear.