The relation of endotoxaemia to the cause of death and fatal hepatic damage following obstruction of the portal vein.
The present study was undertaken in rats with portosystemic collaterals to clarify whether portal vein occlusion induces fatal hepatic damage and whether endotoxaemia relates to development of lethal hepatic failure following portal vein obstruction. Sudden portal vein occlusion caused severe hepatic necrosis and hepatic dysfunction. However, the mortality rate was only 14 per cent, and the hepatic damage recovered 1 week later. Administration of endotoxin immediately after portal vein ligation induced a high mortality rate (86 per cent): the cause of death was thought to be systemic circulatory failure. Endotoxin administration 1 week after portal vein ligation caused marked hepatic dysfunction and hepatic necrosis, but no deaths occurred. These experimental data suggest that hepatic damage following sudden portal vein occlusion is temporary and not fatal provided that portosystemic shunts form adequately. However, it is lethal when complicated by endotoxaemia. Severe hepatic damage and death in chronic portal vein occlusion with portosystemic collaterals cannot be attributed solely to portal vein occlusion, and other factors such as endotoxaemia may play an important role in their development.
Shibayama
Y
Y
Department of Pathology, Osaka Medical College, Japan.
D000818:Animals; D002423:Cause of Death; D004731:Endotoxins / Q000097:blood*; D008026:Ligation; D008099:Liver / Q000473:pathology; D008107:Liver Diseases / Q000209:etiology* / Q000401:mortality / Q000473:pathology; D008111:Liver Function Tests; D008297:Male; D011169:Portal Vein / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains
D004731:Endotoxins