angiotensin-iii and Necrosis

When Escherichia coli endotoxin was intravenously injected into rats given killed Corynebacterium parvum 6 days previously, fibrin deposition and endothelial cell injury occurred in hepatic sinusoids at 1.5 h and were intensified thereafter. Serum alanine aminotransferase values were increased along with prothrombin time and decreased plasma levels of antithrombin III and coagulation factor VIII:C at 5 h. Antithrombin III concentrate (plus heparin) or superoxide dismutase infused concurrently with injection of endotoxin significantly attenuated the derangements of these variables and the histologic extent of liver injury at 5 h. Intravascular coagulation, probably developing through the action of superoxide anion, may contribute to the development of massive hepatic necrosis induced by C. parvum and endotoxin in rats.

Topics: Angiotensin III; Animals; Blood Coagulation; Endothelium, Vascular; Endotoxins; Escherichia coli; Heparin; Liver; Male; Necrosis; Propionibacterium acnes; Rats; Rats, Inbred Strains; Superoxide Dismutase; Time Factors