Enhanced vascular permeability induced in mice by larch arabinogalactan

Abstract

Larch arabinogalactan AG(Lch) enhances vascular permeability when injected into normal mice. Increased vascular permeability is demonstrated by a marked blueing of the ears (BE) which follows the intravenous administration of AG(Lch) and Evans's blue dye. BE can be inhibited by D-galactose, derivatives of D-galactose, and oligosaccharides which contain D-galactose. The stereochemical specificity of inhibition, the specificity of desensitization of mice to AG(Lch) by repeated injections of this polysaccharide and the rapid elimination of [³H]AG(Lch) from the circulation, suggest that AG(Lch) may produce its biological effects by interacting with natural antibody. In vitro oxidation of the terminal non-reducing galactose residues of AG(Lch) by galactose oxidase completely destroys the ear blueing capacity of AG(Lch). BE induced by AG(Lch) in mice resembles anaphylactoid oedema elicited by dextran in rats in that it can be inhibited by the administration of (a) an anti-serotonin drug (UML 491), and (b) a hyperglycaemic inducing agent (alloxan). As in the dextran system in rats, a strain of mice has been found which does not react to AG(Lch).