Friedl H P, Till G O, Trentz O, Ward P A
Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.
Am J Pathol. 1989 Jul;135(1):203-17.
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.
大鼠皮肤烧伤水肿的发病机制似乎与组胺、黄嘌呤氧化酶和氧自由基的作用有关。组胺及其代谢衍生物可提高大鼠血浆和大鼠肺动脉内皮细胞中黄嘌呤氧化酶（而非黄嘌呤脱氢酶）的催化活性。在热损伤大鼠中，血浆组胺和黄嘌呤氧化酶水平平行升高，同时尿酸也增加。用肥大细胞稳定剂色甘酸、补体耗竭剂以及H2受体拮抗剂西咪替丁治疗大鼠，可使烧伤水肿明显减轻，但中性粒细胞耗竭对其无影响。这些研究提示烧伤水肿的发病机制如下：热损伤导致补体激活并释放过敏毒素，肥大细胞分泌组胺，从而增强黄嘌呤氧化酶活性，增加氧自由基的产生，进而损伤内皮细胞。
