Evidence for the involvement of a reperfusion injury in galactosamine/endotoxin-induced hepatitis in mice

作者: Albrecht Wendel , Gisa Tiegs , Christoph Werner

DOI: 10.1016/0006-2952(87)90544-2

关键词: Reperfusion injuryAllopurinolFulminant hepatitisGalactosamineHepatitisImmunologyLiver injuryPharmacologyMedicineProstacyclinSorbitol 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.

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