Regulation of the Pulmonary Circulation During Lung Injury

Abstract

Adult respiratory distress syndrome (ARDS) [1] is not a disease but a disorder which is associated with many clinical states, the most frequent being sepsis, trauma, and aspiration of gastric contents [19]. Less frequently occurring situations are amniotic fluid embolization, acute pancreatitis, radiation lung injury, disseminated intravascular coagulation, and ARDS induced by certain drugs [13]. ARDS was described approximately 20 years ago, yet, since its description the overall mortality has remained stable, indicating that, although some aspects of this syndrome have been studied in various model systems [4–8, 11, 14, 15], the impact of these experiments on patient survival has been very small [2]. Conceptually, ARDS is a massive insult damaging the integrity of the lung membranes. The event which triggers a cascade of metabolic reactions is acute; occasionally the syndrome is rather transient, but most frequently the lung subsequently undergoes a chronic inflammatory phase which leads to cell proliferation and scar tissue formation [19]. The lung circulation is involved in the syndrome since the injurious agents, for example lipopolysaccharide or activated circulating cells, are often carried to the lung via the bloodstream. Pulmonary hypertension has been recognized as part of the syndrome in many patients, as described by Zapol and Snider in 1977 [20]. Morphological studies show obliteration of pulmonary arteries, perivascular edema, and compression of the microcirculation by edema fluid.