Systemic complement activation and acute lung injury.
Experimental studies of rats have provided significant evidence that intravascular complement activation after i.v. injection of cobra venom factor (CVF) or thermal injury of skin can result in acute lung injury. This has been determined by morphological changes in lung and increases in lung vascular permeability. Systemic complement activation is associated with an early appearance of C5-derived chemotactic activity in the circulation coincident with the development of transient neutropenia, followed by extensive granulocytosis and sequestration of neutrophils in lung interstitial capillaries. The acute pulmonary injury depends on availability of complement and neutrophils. Depletion of either complement or blood neutrophils before CVF injection or thermal injury will prevent development of lung injury. Interventional studies with catalase, scavengers of hydroxyl radical OH., and iron chelators have revealed that the acute pulmonary injury is related to production of oxygen-derived free radicals by activated neutrophils. OH. appears to be the key mediator involved in the acute lung microvascular injury.
D000208:Acute Disease; D000818:Animals; D002199:Capillary Permeability / Q000187:drug effects; D003167:Complement Activation / Q000187:drug effects; D003182:Complement C5 / Q000502:physiology; D015936:Complement C5a; D004546:Elapid Venoms / Q000494:pharmacology; D004727:Endothelium / Q000473:pathology; D005609:Free Radicals; D006358:Hot Temperature; D007249:Inflammation / Q000473:pathology / Q000503:physiopathology; D007958:Leukocyte Count; D008168:Lung / Q000098:blood supply / Q000473:pathology*; D009504:Neutrophils / Q000378:metabolism / Q000473:pathology*; D051381:Rats
D003182:Complement C5; D004546:Elapid Venoms; D005609:Free Radicals; D015936:Complement C5a