The pathophysiologic mechanisms of ALI are insufficiently understood. In the common finale of this heterogeneous entity, the alveolo-capillary barrier is compromised allowing consecutive edema formation in the interstitium as well as alveoli, thus compromising gas exchange leading to organ dysfunction and respiratory failure. Histological evaluation of lungs from ALI patients indicated substantial accumulation of activated PMNs, diffuse alveolar damage, loss of epithelial integrity, and increased pulmonary edema (16, 17) . There are several proposed mechanisms which are believed to account for this phenomenon.