In contrast to the defibrination mediated by the thrombin clotting of fibrinogen, such as in the disseminated intravascular coagulation syndrome, the in vivo induction of defibrination by Ancrod or Reptilase is suprisingly benign and not accompanied by significant changes in most clotting factors or in platelet count. This difference was studied in vitro using an approach based on the structural differences between the thrombin induced fibrin and fibrin formed by Ancrod and Reptilase. The latter two varieties of fibrin were shown to be more susceptible to plasmin proteolysis. In addition, the resulting breakdown products were found to be of smaller molecular sizes than those produced by proteolysis of thrombin induced fibrin. Investigations of biological activities of these fibrinogen derivatives including their anticoagulant effect and its inhibition of platelet aggregation supports this concept.
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