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Pulmonary microvascular alterations and injury induced by complement fragments: synergistic effect of complement activation, neutrophil sequestration, and prostaglandins.

Authors
  • Henson, P M
  • Larsen, G L
  • Webster, R O
  • Mitchell, B C
  • Goins, A J
  • Henson, J E
Type
Published Article
Journal
Annals of the New York Academy of Sciences
Publication Date
Jan 01, 1982
Volume
384
Pages
287–300
Identifiers
PMID: 6953825
Source
Medline
License
Unknown

Abstract

Fragments of C5 that are generated at, or administered to, extravascular sites in the pulmonary parenchyma induced neutrophil infiltration, edema, tissue damage, and a complete inflammatory response. Generation of C5 fragments within the vascular system induced leukocyte sequestration in the pulmonary vasculature, but without detectable increased vascular permeability or neutrophil migration. By contrast, the combination of short episode of hypoxemia with the intravascular C5 activation led significant increases in pulmonary vascular permeability, mild endothelial alterations, and emigration of neutrophils. Infusion of 10 micrograms PGE2 into animals in which intravascular complement had been activated produced changes in the lungs that were similar to, though less severe than, the combination of hypoxia and complement activation.

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