Lung injury secondary to chemotactic factor-induced leukocyte activation.
Intravascular complement activation in rats following thermal injury or vascular infusion of cobra venom factor results in acute lung injury as determined morphologically and measured by increases in lung vascular permeability. The acute lung injury is associated with the early appearance of C5-derived chemotactic activity in the circulation coincident with the development of neutropenia. The lung injury is closely linked to availability of complement and neutrophils and can be prevented by systemic treatment of animals with a combination of superoxide dismutase and catalase, specific inhibitors of toxic oxygen metabolites. These data suggest that intravascular complement activation leads to activation of neutrophils and their intrapulmonary capillary sequestration, and subsequent acute lung injury, which is associated with production and release of oxygen-derived free radicals by C5a-activated blood neutrophils.
D000818:Animals; D002199:Capillary Permeability; D002374:Catalase / Q000494:pharmacology; D002630:Chemotactic Factors / Q000502:physiology*; D002634:Chemotaxis, Leukocyte; D003167:Complement Activation; D003182:Complement C5 / Q000502:physiology; D015936:Complement C5a; D004195:Disease Models, Animal; D006801:Humans; D008168:Lung / Q000098:blood supply; D008171:Lung Diseases / Q000209:etiology* / Q000517:prevention & control; D009504:Neutrophils / Q000502:physiology; D051381:Rats; D013482:Superoxide Dismutase / Q000494:pharmacology
D002630:Chemotactic Factors; D003182:Complement C5; D015936:Complement C5a; D002374:Catalase; D013482:Superoxide Dismutase