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PULMONARY MICROVASCULAR ALTERATIONS AND INJURY INDUCED BY COMPLEMENT FRAGMENTS: SYNERGISTIC EFFECT OF COMPLEMENT ACTIVATION, NEUTROPHIL SEQUESTRATION, AND PROSTAGLANDINS *
Author(s) -
Henson Peter M.,
Larsen Gary L.,
Webster Robert O.,
Mitchell Brenda C.,
Goins Alan J.,
Henson Jan E.
Publication year - 1982
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1982.tb21379.x
Subject(s) - complement (music) , complement system , chemistry , pulmonary injury , immunology , lung , medicine , biochemistry , antibody , pulmonary fibrosis , complementation , gene , phenotype
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.