Intravascular activation of complement and XXXX . Dependency on neutrophils and toxic @entity26 metabolites.

@entity1 @entity16206 @entity548 @entity26 @entity651 @entity3900 @entity1398 @entity2242 @entity358 @entity2196 @entity1317 @entity224 @entity647
Intravascular activation of the complement system with cobra venom factor results in @entity647 , which has been quantitated by increases in lung vascular permeability. Cobra venom factor preparations devoid of @entity3900 activity retain full lung-damaging capacity. The @entity651 is associated with the preceding appearance of chemotactic activity in the serum coincident with the development of a profound @entity1398 . The chemotactic activity is immunochemically related to @entity1 @entity2242 . Morphologic studies have revealed discontinuities in the endothelial cell lining of @entity358 , damage and/or destruction of endothelial cells in these areas, plugging of @entity358 with neutrophils that are in direct contact with vascular basement membrane, the presence of fibrin in alveolar spaces and in areas adjacent to damaged endothelial cells, and @entity548 . @entity651 is dramatically attenuated in animals that have been previously neutrophil depleted. Teh intravenous injection of @entity224 dismutase or @entity2196 also provides significant protection from the @entity358 . Very little protection from the @entity358 . Very little protection is afforded by pretreatment of rats with @entity16206 . These studies suggest that intravascular activation of the complement system leads to neutrophil aggregation and activation, intrapulmonary capillary sequestration of neutrophils, and @entity1317 , which may be related to production of toxic @entity26 metabolites by complement-activated neutrophils.
