Experimental hepatic necrosis: studies on coagulation abnormalities, plasma clearance, and organ distribution of 125I-labelled fibrinogen.
Studies in the rat with hepatic necrosis induced by carbon tetrachloride showed that the abnormalities in one-stage coagulation tests and the increased catabolism of fibrinogen were similar to those found in man with acute viral or drug-induced hepatic necrosis. Determination of the distribution of the radioactive label shows that excessive deposition was maximal in the liver but also occurred in the spleen. The appearance is delayed by heparin but accelerated by tranexamic acid.
D000818:Animals; D000933:Antifibrinolytic Agents; D001778:Blood Coagulation Disorders / Q000503:physiopathology*; D001780:Blood Coagulation Tests; D001835:Body Weight; D002251:Carbon Tetrachloride; D056486:Chemical and Drug Induced Liver Injury; D003509:Cyclohexanecarboxylic Acids; D005260:Female; D005340:Fibrinogen / Q000032:analysis / Q000378:metabolism*; D006400:Hematocrit; D006493:Heparin; D007456:Iodine Isotopes; D008099:Liver / Q000032:analysis; D008107:Liver Diseases / Q000473:pathology / Q000503:physiopathology*; D009336:Necrosis / Q000503:physiopathology*; D009929:Organ Size; D011517:Prothrombin Time; D051381:Rats
D000933:Antifibrinolytic Agents; D003509:Cyclohexanecarboxylic Acids; D007456:Iodine Isotopes; D005340:Fibrinogen; D006493:Heparin; D002251:Carbon Tetrachloride