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Thromb Haemost 1967; 17(01/02): 065-077
DOI: 10.1055/s-0038-1654112
Originalarbeiten - Original Articles - Travaux Originaux
Schattauer GmbH

Soluble Unclottable Complexes Formed in the Presence of Fibrinogen Degradation Products (FDP) during the Fibrinogen-Fibrin Conversion and Their Potential Significance in Pathology

B Lipinski
1   Department of Radiobiology and Health Protection, Institute of Nuclear Research, Warsaw, 9, Poland
,
Z Wegezynowicz
1   Department of Radiobiology and Health Protection, Institute of Nuclear Research, Warsaw, 9, Poland
,
A. Z Budzynski
1   Department of Radiobiology and Health Protection, Institute of Nuclear Research, Warsaw, 9, Poland
,
Maria Kopeć
1   Department of Radiobiology and Health Protection, Institute of Nuclear Research, Warsaw, 9, Poland
,
Z. S Latallo
1   Department of Radiobiology and Health Protection, Institute of Nuclear Research, Warsaw, 9, Poland
,
E Kowalski
1   Department of Radiobiology and Health Protection, Institute of Nuclear Research, Warsaw, 9, Poland
› Author Affiliations
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Publication History

Publication Date:
26 June 2018 (online)

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Summary

1. With the aid of isotopie technique, it was shown, that fibrinogen, fibrinogen-fibrin intermediates and fibrinogen degradation products (FDP) may form soluble complexes, which are unclottable by thrombin.

2. These complexes may be precipitated by protamine sulphate or by cooling to 4° C (par a coagulation),

3. The above findings are discussed in regard to their significance in the pathology of the acute defibrination syndrome :

a) Paracoagulation by protamine sulphate without addition of thrombin occurs when defibrination is caused by excessive intravascular clotting, while in cases of the syndrome due to proteolytic digestion of fibrinogen, paracoagulation occurs after combined action of thrombin and protamin sulphate.

b) Formation of the complexes described above may explain the occurence of cryofibrinogens in various pathological states.

c) Formation of these complexes is postulated to be an important factor involved in the development of the hemostatic defect. It may be as well the expression of a defence mechanism against intravascular fibrin formation by rendering unclottable the intermediates of the fibrinogen-fibrin conversion.

 

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