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Fibrinolytic System in Certain Congenital and Hereditary Hæmorrhagic Disorders: a Critical Evaluation of the Theory of Dynamic Hæmostasis

Nature volume 200, pages 478–479 (1963)Cite this article

Abstract

MOLE1 has directed attention to the possible physiological role of fibrinolysis in preventing thrombi from being formed on the vascular endothelium and suggested that atherosclerosis might result from the failure of this defence mechanism. Copley2,3 postulated that, in vivo, there existed a dynamic equilibrium between two opposing forces, one depositing fibrin on the vascular endothelium (the coagulation mechanism) and the other constantly removing it (the fibrinolytic mechanism). A balanced harmony between the two processes maintains the integrity of the vascular endothelium and accordingly an, imbalance might result in abnormal fibrin deposition, leading on one hand to atherosclerosis and/or to thrombus formation, and on the other to a hæmorrhagic state. This view has been supported by other workers4–7 for it has offered an attractive explanation of the patho-genesis of thromboembolic syndromes. Added support has been the findings of a decreased ‘fibrinolytic activity’ after myocardial infarction, intermittent claudication8 and after fatty meals9.

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Author notes

  1. KARIM KAMEL

    Present address: On a study grant from Ain-Shams University, Cairo

Authors and Affiliations

  1. Edinburgh and South-East Scotland Blood Transfusion Service, Department of Hæmatology, Royal Infirmary, Edinburgh

    KARIM KAMEL, R. A. CUMMING & S. HOWARD DAVIES

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KAMEL, K., CUMMING, R. & HOWARD DAVIES, S. Fibrinolytic System in Certain Congenital and Hereditary Hæmorrhagic Disorders: a Critical Evaluation of the Theory of Dynamic Hæmostasis. Nature 200, 478–479 (1963). https://doi.org/10.1038/200478b0

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