ABSTRACT
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.
Subject(s)
Blood Coagulation Disorders/physiopathology , Fibrinogen/metabolism , Liver Diseases/physiopathology , Necrosis/physiopathology , Animals , Antifibrinolytic Agents , Blood Coagulation Tests , Body Weight , Carbon Tetrachloride , Chemical and Drug Induced Liver Injury , Cyclohexanecarboxylic Acids , Female , Fibrinogen/analysis , Hematocrit , Heparin , Iodine Isotopes , Liver/analysis , Liver Diseases/pathology , Organ Size , Prothrombin Time , RatsABSTRACT
The effect of heparin therapy was followed in 50 patients treated for thrombo-embolic disease. Individual response to a standard dose of 40,000 units of heparin daily showed a considerable variation and the effect was not constant on subsequent days. Five of the 50 patients developed a serious haemorrhage. It is proposed that to ensure the adequacy of treatment detectable levels of heparin should be obtained but because of the high risk of bleeding these levels should not be excessive. The results suggest that control of heparin therapy can be based on the thrombin clotting time. Using this test it is advised that treatment is monitored daily in order to achieve a plasma heparin level of up to 1 mg per 100 ml.
