[Hemostatic-vascular interactions in the pathogenesis and the treatment of adult respiratory distress syndrome].

The complex pathophysiologic alterations occurring in adult respiratory distress syndrome (ARDS) result from the interaction of various humoral and cellular mediators. In this review we examine the events that lead to acute pulmonary injury as discussed in the recent literature as well as the correlations among humoral systems and cell activation involved in the pathogenesis of ARDS. We also consider the mechanisms inducing the appearance of adhesive molecules (ELAM-1 and ICAM-1) on the surface of endothelial cells, the importance of complement and clotting activation, and the role of monocyte-macrophages, platelets and neutrophils. The complexity of alterations among the different mediators involved in the pathogenesis of ARDS is underscored by experimental results demonstrating how the pharmacologic blockade of each system cannot completely prevent the development of lung damage. Understanding of the complex processes involved in the pathogenesis of ARDS provides new prospects for its treatment, such as inhalational nitric oxide and aerosolised prostacyclin. The most promising approach involves the use of monoclonal antibodies which may enable the selective inhibition of different mediators and endotoxins.