Roles of histamine, complement and xanthine oxidase in thermal injury of skin

• Published in: The American journal of pathology Vol. 135; no. 1; pp. 203 - 217
• Main Authors: Friedl, HP, Till, GO, Trentz, O, Ward, PA
• Format: Journal Article
• Language: English
• Published: Bethesda, MD ASIP 01-07-1989; American Society for Investigative Pathology
• Subjects: Animals; Biological and medical sciences; Burns; Burns - complications; Burns - enzymology; Burns - metabolism; Cimetidine - pharmacology; Complement Inactivator Proteins - pharmacology; Complement System Proteins - metabolism; Cromolyn Sodium - pharmacology; Edema - enzymology; Edema - etiology; Edema - metabolism; Elapid Venoms - pharmacology; Endothelium, Vascular - metabolism; Histamine - metabolism; Histamine H1 Antagonists - pharmacology; Hydroxides; Hydroxyl Radical; Kinetics; Male; Medical sciences; Radioimmunoassay; Rats; Skin - injuries; Skin - metabolism; Superoxides - metabolism; Traumas. Diseases due to physical agents; Uric Acid - biosynthesis; Uric Acid - blood; Xanthine Oxidase - blood; Xanthine Oxidase - metabolism; Skin disease; Rat; Pathogenesis; Rodentia; Complement; Trauma; Burn; Histamine; Vertebrata; Experimental disease; Mammalia; Animal; Xanthine oxidase; Skin
• ISSN: 0002-9440; 1525-2191

The pathogenesis of burn edema in the skin of rats appears to be related to a role for histamine, xanthine oxidase and oxygen radicals. Histamine and its metabolic derivatives increase the catalytic activity of xanthine oxidase (but not xanthine dehydrogenase) in rat plasma and in rat pulmonary artery endothelial cells. In thermally injured rats levels of plasma histamine and xanthine oxidase rise in parallel, in association with increases in uric acid. Burn edema is greatly attenuated by treatment of rats with the mast cell stabilizer, cromolyn, by complement depletion and by treatment with the H2 receptor antagonist, cimetidine, but is unaffected by neutrophil depletion. These studies suggest the following pathogenesis of burn edema: thermal trauma causes complement activation with anaphylatoxin release and mast cell secretion of histamine, leading to enhancement of xanthine oxidase activity and increased production of oxygen radicals which damage endothelial cells.