Effect of streptokinase on hemostasis.

The effect of streptokinase on hemostasis was studied by direct observation of hemostatic plugs in the rabbit mesentery. Infusion of streptokinase did not produce dissolution of hemostatic plugs which were already formed. It did cause a delay in the formation of a platelet mass capable of arresting bleeding from injured vessels. In contrast to systemic infusion, topical application of streptokinase did produce disruption of hemostatic plugs which were already formed. Comparison of the electronmicroscopic appearances of plugs from the control and streptokinase infused animals revealed a lack of fibrin around the plugs in the streptokinase treated animals but no significant difference in platelet morphology. In vitro tests with ADP, thrombin and collagen on platelet-rich plasma from the streptokinase infused animals did not show any difference in platelet aggregation between the pre-and postinfusion samples, even though streptokinase infusion produced a marked increase in plasma fibrinolytic activity. It is suggested that streptokinase infusions, which produce only a slight fall in the plasma fibrinogen level, impair hemostatic plug formation by digestion of fibrin as it is formed around the aggregated platelets.

[1]  H. Rowsell,et al.  Experimental hemostasis in normal dogs and dogs with congenital disorders of blood coagulation. , 1967, Blood.

[2]  J. Mustard,et al.  ALTERATION OF THE RESPONSE OF PLATELETS TO SURFACE STIMULI BY PYRAZOLE COMPOUNDS , 1967, The Journal of experimental medicine.

[3]  A. Fletcher,et al.  EFFECT OF FIBRIN AND FIBRINOGEN PROTEOLYSIS PRODUCTS ON CLOT PHYSICAL PROPERTIES. , 1965, The American journal of physiology.

[4]  A. Fletcher,et al.  THE DEVELOPMENT OF UROKINASE AS A THROMBOLYTIC AGENT. MAINTENANCE OF A SUSTAINED THROMBOLYTIC STATE IN MAN BY ITS INTRAVENOUS INFUSION. , 1965, The Journal of laboratory and clinical medicine.

[5]  Z. Wegrzynowicz,et al.  Studies on the Molecular Pathology and Pathogenesis of Bleeding in Severe Fibrinolytic States in Dogs , 1964, Thrombosis and Haemostasis.

[6]  H. Rowsell,et al.  EFFECT OF ADENOSINE NUCLEOTIDES ON PLATELET AGGREGATION AND CLOTTING TIME. , 1964, The Journal of laboratory and clinical medicine.

[7]  A. Budzynski,et al.  Inhibition of Thrombin and of Fibrin Polymerization, Two Activities derived from Plasmin-digested Fibrinogen , 1964, Nature.

[8]  T. Hovig.  Aggregation of Rabbit Blood Platelets Produced in Vitro by Saline “Extract” of Tendons , 1963, Thrombosis and Haemostasis.

[9]  A. Fletcher,et al.  Pathogenesis of the coagulation defect developing during pathological plasma proteolytic ("fibrinolytic") states. II. The significance, mechanism and consequences of defective fibrin polymerization. , 1962, The Journal of clinical investigation.

[10]  A. Fletcher,et al.  Pathogenesis of the coagulation defect developing during pathological plasma proteolytic ("fibrinolytic") states. I. The significance of fibrinogen proteolysis and circulating fibrinogen breakdown products. , 1962, The Journal of clinical investigation.

[11]  A. Fletcher,et al.  Pathogenesis of the coagulation defect developing during pathological plasma proteolytic ("fibrinolytic") states. III. Demonstration of abnormal clot structure by electron microscopy. , 1962, The Journal of clinical investigation.

[12]  A. Fletcher,et al.  The mechanism of clot dissolution by plasmin. , 1959, The Journal of clinical investigation.

[13]  A. Fletcher,et al.  The maintenance of a sustained thrombolytic state in man. I. Induction and effects. , 1959, The Journal of clinical investigation.

[14]  Oliver H. Lowry,et al.  Protein measurement with the Folin phenol reagent. , 1951, The Journal of biological chemistry.

[15]  Z. Wegrzynowicz,et al.  Influence of Fibrinogen Degradation Products (FDP) on Platelet Aggregation, Adhesiveness and Viscous Metamorphosis , 1963, Thrombosis and Haemostasis.