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Acute Disseminated Intravascular Coagulation and Fibrinolysis

Arch Surg. 1964;88(4):694-698. doi:10.1001/archsurg.1964.01310220184028.
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There is substantial evidence that the clotting mechanism is normally engaged in the prevention of abnormal bleeding or, stated in another way, that its dynamic activity is essential for the preservation of the integrity of the normal circulation.1 Evidence for a dynamic status of blood coagulation has been previously described,2 though the precise means by which a continuing coagulation at carefully regulated rates prevents abnormal bleeding from the microcirculation on the one hand and avoids intravascular coagulation on the other is not fully understood.

An intriguing process in this connection is that of fibrinolysis which, like other enzymatic processes in vivo, also proceeds at homeostatic rates under normal or resting states. However, its rates may be greatly accelerated by activators or kinases which catalyze the conversion of profibrinolysin to fibrinolysin, and under these conditions part or all of the circulating fibrinogen may be destroyed.

Fibrinolysin is a proteolytic


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