In 1967, Ashbaugh and associates (1) described the development of acute respiratory failure in 12 patients with tachypnea, hypoxemia, and a loss of lung compliance who did not respond to the usual respiratory therapy. Post-mortem examination of the lungs of seven of these patients revealed atelectasis, hemorrhage, pulmonary edema, and hyaline membrane formation. The clinical and pathologic features were feit to resembie those seen in premature infants with the respiratory distress syndrome (RDS). They postulated that the surface active material lining the alveoli was abnormal and contributed to the pathophysiology of the respiratory failure. Shortlythereafter, Petty and Ashbaugh proposed that this entity be called the adult respiratory distress syndrome (ARDS)(2). Since then, there has been extensive research of the pathogenesis and clinical outcome of patients with ARDS. It is now feit that although a variety of different insuits may lead to ARDS, a common final pathway results in alveolar damage (2-5). This pathway may include complement and leukocyte activation within lung tissue with the release of oxygen free radicals and inflammatory mediators such as interleukin-1 (IL-1), proteases, and tumor necrosis factor (TNF)(6-8). Their involvement is inferred from data report-