Cannulation of the thoracic duct and femoral vein in dogs was performed so that samples could be taken at intervals. Lymph fibrinolytic factors (especially plasminogen activator, plasminogen and antiplasmin) and the influence of urokinase administered intravenously by one shot on thoracic duct lymph fibrinolysis were studied in dogs weighing 10 kg.Results were as follows. Plasminogen activator, plasminogen and antiplasmin are presented in lymph. Levels of plasminogen in thoracic duct lymph were lower than in blood, but there was no significant difference in antiplasmin levels between in blood and lymph. Lymph plasminogen activator levels were variable and changes of lymph fiibrinolytic activity were not definitive after the administration of 120, 000 units of urokinase. Antiplasmin levels, however, reduced transiently in lymph as well as in blood. The highest radio activity in lymph was seen 30 minutes after administration of 125I-labeled urokinase. Administration of urokinase seemed to increase thoracic duct lymphatic flow, but there was no statistical difference.
We have experienced two cases of DIC following infusion of ascitic fluid from the peritoneal cavity to the vascular system. We have studied the etiology of this DIC. So, FDP, endotoxin, coagulant factors and procoagulant activity were investigated in ascitic fluid of 11 hepatic cirrhosis cases and 15 cancer cases.Method and Result; FDP in ascites were more included than in plasma. Endotoxin were positive in about 60% of ascitic fluid. The coagulant factors were recognized a littile except VUI-factor. Only ascitic fluid ded not clott the fibrinogen and did not affect the platlate aggregation. The procoagulant activities were measured by clotting times which the normal plasma (0.lcc) was added with the ascitic fluid or buffer (0.1cc), after 3 minutes incubation, and then added with 1/40 M Cacl2 (0.1cc).The clotting time was shortened in the ascitic fluid than buffer (buffer 120.7 ± 7.9 sec, Cancer 82 ± 23.8 sec., cirrhosis 91.4 ± 16.5 sec), and both VII and VIII deficient plasma was shortened too, but X dificient plasma was not coagulated. Also FDP and endotoxin did not shorten the clotting time of normal plasma. Experimentally, the ascitic fluid in dog by binding vena cava in ferior and the ascitic fluid in rat by transplantation of tumor cells shortened the clotting time. Conclusion; Coagulant, fibrinolytic and procoagulant factors were existed in ascitic fluid. We think that DIC induced by ascitic fluid are due to this procoagulant factor and this procoagulant factor may be not tissue - thromboplastin only.
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