作者: Albrecht Wendel , Gisa Tiegs , Christoph Werner
DOI: 10.1016/0006-2952(87)90544-2
关键词: Reperfusion injury 、 Allopurinol 、 Fulminant hepatitis 、 Galactosamine 、 Hepatitis 、 Immunology 、 Liver injury 、 Pharmacology 、 Medicine 、 Prostacyclin 、 Sorbitol dehydrogenase
摘要: Simultaneous intraperitoneal administration of 700 mg/kg galactosamine and 33 micrograms/kg Salmonella abortus equi endotoxin to male NMRI albino mice resulted in fulminant hepatitis as assessed after nine hours by measurement serum transaminases well sorbitol dehydrogenase activities. Intraperitoneal pretreatment animals with 2 X 100 allopurinol, or intravenous kU superoxide dismutase 1 MU catalase fully prevented hepatitis. Administration 10 the prostacyclin analogue iloprost antagonized liver injury when given simultaneously galactosamine/endotoxin but did not protect 90 min later. Tocopherol desferal had no significant protective effect. Together our recent finding that hepatic leukotriene D4 production is likely be responsible for galactosamine/endotoxin-induced we interpret these results evidence a leukotriene-induced ischemia followed reperfusion syndrome.