Kind L S, Macedo-Sobrinho B, Ako D
Immunology. 1970 Nov;19(5):799-807.
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 [H]AG(Lch) from the circulation, suggest that AG(Lch) may produce its biological effects by interacting with natural antibody. 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).
落叶松阿拉伯半乳聚糖（AG[Lch]）注入正常小鼠后可增强血管通透性。静脉注射AG[Lch]和伊文思蓝染料后，耳朵明显变蓝（BE）表明血管通透性增加。BE可被D-半乳糖、D-半乳糖衍生物以及含有D-半乳糖的寡糖抑制。抑制的立体化学特异性、通过重复注射该多糖使小鼠对AG[Lch]脱敏的特异性以及[H]AG[Lch]从循环中的快速清除，表明AG[Lch]可能通过与天然抗体相互作用产生其生物学效应。半乳糖氧化酶对AG[Lch]末端非还原半乳糖残基的氧化完全破坏了AG[Lch]的耳朵变蓝能力。AG[Lch]在小鼠中诱导的BE类似于右旋糖酐在大鼠中引发的类过敏水肿，因为它可被以下物质抑制：（a）一种抗血清素药物（UML 491），以及（b）一种高血糖诱导剂（四氧嘧啶）。与大鼠的右旋糖酐系统一样，已发现一种小鼠品系对AG[Lch]无反应。
