Mechanisms of acute lung injury.
The role of the complement system in generating an acute inflammatory response in the lung, manifested particularly by the presence of neutrophils, and the role of these neutrophils in altering lung microvascular permeability are examined. Although it is not possible at this time to reconcile all the experimental data so as to provide a unifying hypothesis of the pathogenesis of acute lung injury, the mechanisms discussed in this article provide clues not only about lung injury itself, but also about the basic mechanisms of inflammation.
D000208:Acute Disease; D000328:Adult; D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism; D002199:Capillary Permeability; D002448:Cell Adhesion; D002465:Cell Movement; D005609:Free Radicals; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D008168:Lung / Q000098:blood supply / Q000276:immunology / Q000473:pathology*; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism / Q000502:physiology; D010101:Oxygen Consumption; D010447:Peptide Hydrolases / Q000378:metabolism; D012128:Respiratory Distress Syndrome / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology
D001095:Arachidonic Acids; D005609:Free Radicals; D010447:Peptide Hydrolases