ANTAGONISTS TO HEMOSTASIS

Both platelet activation and coagulation are self-
perpetuating processes that could potentially
continue until an injured vessel is completely
occluded. Coagulation inhibitors are present to
prevent excessive clotting and to dissolve the clot as
tissue repair occurs.
Maintaining adequate blood flow aids in diluting
and removing clotting factors and in dispersing
aggregated platelets. Partially activated coagulation
factors are carried to the liver and the reticuloen-
dothelial system, where they are degraded.

Two specific anticoagulation mechanisms also help to
prevent excessive clotting: (1) the fibrinolytic system
and (2) the antithrombin system.
In the fibrinolytic system, fibrin strands are
broken down into progressively smaller fragments
by a proteolytic enzyme, plasmin. Although plasmin
does not circulate in active form, its precursor, plas-
minogen, does. Plasminogen is converted into plas-
min by several plasminogen activators, among them
factor XII, urokinase, and streptokinase. Once acti-
vated, plasmin digests fibrin, splits fibrinogen into
peptide fragments (fibrin split products [FSP]), and
degrades factors V, VIII, and XIII. In addition, the
FSP interfere with platelet aggregation, reduce
prothrombin, and interfere with conversion of solu-
ble fibrin to insoluble fibrin. Plasma also contains
agents that neutralize plasmin itself. Among these
are antiplasmin and
1-antitrypsin. A balance
between proplasmin and antiplasmin substances
aids in maintaining normal coagulation.