Thromb Haemost 1963; 09(02): 427-435
DOI: 10.1055/s-0038-1654995
Originalarbeiten — Original Articles — Travaux Originaux
Schattauer GmbH

Experimental Venous Thrombosis in Rats

Increased Formation During Inhibition of the Fibrinolytic System with Epsilon Amino Caproic Acid
Arne Nordöy*
1   Institute for Thrombosis Research (Head: P. A. Owren, M. D.), University Hospital, Rikshospitalet, Oslo, Norway
› Institutsangaben
Weitere Informationen

Publikationsverlauf

Publikationsdatum:
21. Juni 2018 (online)

Summary

1. Thrombosis in rats were produced by Blake et al.’s technique of application of formalin solution to the jugular vein. The incidence of thrombosis produced by a 10% (v/v) formalin in 65% methanol solution and observed after 24 hours was 30% ± 4.6 S. D.

2. The administration of 100 mg EACA 1,000 g body weight orally every fourth hour for 24 hours increased the incidence of thrombosis about twice (to about 65%).

A single dose of 400 mg EACA 1,000 g body weight had a slight effect only.

3. EACA increased markedly the antifibrinolytic activity in plasma with a maximum after 3—5 hours oral administration. A moderate increase in the fibrinogen concentration was observed in all groups.

4. Global tests for plasma coagulation, the platelet count and the number of adhesive platelets were not significantly influenced by the administration of EACA.

* Research fellow of the Norwegian Council on Cardiovascular Diseases.


 
  • References

  • Ablondi F. B, De Renzo E. C. Mechanism of clot lysis by streptokinase and effects of å-aminocaproic acid. Proc. Soc. exp. Biol. (N. Y) 102: 717-719 1959;
  • Alkjaersig N, Fletcher A. P, Sherry S. å-aminocaproic acid: Inhibitor of plasminogen activation. J. biol. Chem. 234: 832-837 1959;
  • Ashwin J. G. The effect of drugs on experimental thrombosis. Anticoagulants and fibrinolysis. 117-127 MacMillan, Canada: 1961
  • Blake O. R, Ashwin J. G, Jaques L. B. An assay for the antithrombotic activity of anticoagulants. J. clin. Path. 12: 118-122 1959;
  • Blombäck B, Blombäck M. Purification of human and bovine fibrinogen. Ark. Kemi. 10: 415 1956;
  • Egeberg O. Assay of antihemophilic A, B and C factors by one-stage cephalin systems. Scand. J. clin. Lab. Invest. 13: 140-152 1961;
  • Godai H. C. Quantitative and qualitative changes in fibrinogen following major surgical operations. Acta med. scand. 171: 687-694 1962;
  • Goctal H. C. Simple syneresis procedure for fibrinogen assay. Scand. J. clin. Lab. Invest. 13: 530-530 1961;
  • Hellem A. J. The adhesiveness of human blood platelets in vitro. Scand. J. clin. Lab. Invest. 12 Suppl. 51 1960;
  • Hjort P. F, Rapaport S. I, Owren P. A. A simple specific one stage prothrombin assay using Russell’s viper venom in cephalin suspension. J. Lab. clin. Med. 46: 89-97 1955;
  • Hjort P. F. Intermediate reactions in the coagulation of blood with tissue thromboplastin. Scand. J. clin. Lab. Invest. 09 Suppl. 27 1957;
  • Jacobsson K. Studies on trypsin and plasmin inhibitors in human blood serum. Scand. J. clin. Lab. Invest. 07: 55-102 1955;
  • Jacobsson K. Studies on the determination of fibrinogen in human blood plasma. Scand. J. clin. Lab. Invest. 07 Suppl. 14 1955;
  • Lang K, Bitz H. Über den Stoffwechsel der å-Aminocaproicsäure. Biochem. Z. 324: 495-498 1953;
  • McNicol G. P, Fletcher A. P, Alkjaersig N, Sherry S. Impairment of hemostasis in the urinary tract: the role of urokinase. J. Lab. clin. Med. 58: 34-46 1961;
  • Naeye R. L. Thrombotic state after a hemorrhagic diathesis, a possible complication of therapy with å-aminocaproic acid. Blood 19: 694-701 1962;
  • Naeye R. L. Thrombotic disorders with increased levels of antiplasmin and antiplasminogen. New Engl. J. Med. 265: 867-871 1961;
  • Nilsson I. M, Sjoerdsma A, Waldenström J. Antifibrinolytic activity and metabolism of å-aminocaproic acid. Lancet. II: 1322-1326 1960;
  • Nilsson I. M, Björkman S. E, Andersson L. Clinical experiences with å-aminocaproic acid as an antifibrinolytic agent. Acta med. scand. 170: 487-509 1961;
  • Nygaard K. K. A direct method of counting platelets in oxalated plasma. Proc. Mayo Clin. 08: 365-370 1933;
  • Owren P. A. The coagulation of blood. Investigations on a new clotting factor. Acta med. scand. 128 Suppl. 194 327 1947;
  • Owren P. A, Aas K. The control of dicumarol therapy and the quantitative determination of prothrombin and proconvertin. Scand. J. clin. Lab. Invest. 03: 201-208 1951;
  • Phillips L. L, Skrodelis V. Fibrinolytic enzym system in normal, haemorrhagic and disease states. J. clin. Invest. 37: 965-973 1958;
  • Samuels P. B, Webster D. R. The role of venous endothelium in the inception of thrombosis. Amer. Surg. 136: 422-438 1952;
  • Sandberg H, Tsitouris G, Bellet S. Experiences with inhibitors to plasminplasminogen system in human subject: their modification by thrombolysin therapy. Amer. J. Cardiol. 06: 432-438 1960;
  • Sherry S, Fletcher A. P, Alkjaersig N, Sawyer W. D. å-aminocaproic acid. A potent inhibitor of plasminogen activation. Trans. Ass. Amer. Physiol. 72: 62-68 1959;
  • Tasaka S, Abe T. Fibrinolysis and its clinical significance. Asian med. J. 03: 378-382 1960;
  • Waaler B. A. Contact activation in the intrinsic blood clotting system. Thesis. Scand. J. clin. Lab. Invest. 11 Suppl. 37 1959;