THE EFFECT OF STREPTOKINASE ON THE PLATELET AGGREGATES IN ARTIFICIAL <i>IN VITRO</i> THROMBOSIS

Mc, Rozenberg

doi:10.1038/icb.1965.23

Cited by 4 publications

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“…Other work showing that platelet masses are formed normally in vitro in the cone in cone viscometer in the presence of streptokinase stimulation of fibrinolysis and the resistance of these platelet masses to this process although fibrinolysis (Rozenberg 1965) is at variance with these findings and at present remains unexplained. The occasional presence of a qualitative platelet defect in various malignant disorders of the blood has been inferred in the past (Perry 1957, Friedman et al 1964, but is demonstrated in the present study.…”

Section: Discussionmentioning

confidence: 92%

The Rate of Platelet Aggregation in Haemorrhagic Disease and Thrombosis

Firkin

1966

Scandinavian Journal of Haematology

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The degree of platelet aggregation in healthy subjects, haemorrhagic disease and thrombosis has been studied by means of two techniques. Firstly, using a small cone in cone viscometer at high rates of shear, an artificial in vitro thrombus was obtained which represents aggregation of platelets during the process of coagulation. Secondly, a turbidiometric method measuring the fall in optical density during aggregation of platelets was used to record the rate of platelet cohesion in the presence of adenosine diphosphate (ADP) or thrombin. There was rough correlation between the effects of thrombin and ADP on the rate of aggregation in various normal subjects suggesting that the mechanism in the presence of these two substances was similar. The rate of platelet aggregation was observed weekly in ten normal females and no change occurred at the onset of menstruation. Platelet aggregation was found normal in factor VIII deficiency, factor IX deficiency, moderate factor VII deficiency, hypofibrinogenaemia as well as in patients on phenindione or heparin. Impaired aggregation was due to a specific platelet defect in some leukaemias, reticuloses, uraemia as well as two cases of Glanzmann's disease. The defect in aggregation in Waldenström's macroglobulinaemia and fibrinolysis appeared to be due to a plasma factor. Our present method of study did not reveal any abnormality in two cases of von Willebrand's disease and appear insensitive to lack of “Anti‐Willebrand factor”. The study of patients with arterial or venous thrombosis produced values wholly within the normal range and no evidence for a state of “increased tendency to aggregation” was obtained.

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Section: Discussionmentioning

confidence: 92%