LEUCOCYTES AND PULMONARY MICROVASCULAR INJURY

Indirect injury to the lung’s endothelial barrier due to interaction between physical and chemical agents with elements in circulating blood is receiving increased attention since it may be amenable to early treatment. Several types of acute lung injury may have common final pathways, involving the clotting system, platelets, immune mechanisms, or leucocytes. Progress in the last several years has been rapid as clinicians, hematologists, immunologists, pathologists, and physiologists have recognized that acute lung microvascular injury may result from supposedly normal defense mechanisms. Lung pathologists have recognized similarities in the lungs of patients dying of the adult respiratory distress syndrome even though the syndrome was triggered by disparate insults.’-3 In addition to interstitial and alveolar edema with hyaline membranes, there is evidence of widespread microembolization and neutrophil sequestration and infiltration. In 1974 we reported that acute neutropenia occurs in sheep during Pseudomonos bacteremia, followed in a few hours by a marked increase in lung microvascular permeability to fluid and protein.‘ Similar correlations between acute neutropenia or sequestration of neutrophils and in the lung’s microcirculation and acute lung injury have been noted in E. coli ~ept icemia.~ following hemodialysis,6 in immune complex injury.? after pulmonary microembolization,8 in trauma and shock.’ and in the terminal phase of oxygen toxicity.”