Clot restriction prevents the clot from forming in inappropriate areas. Clot breakdown occurs after healing has occurred. The top illustration represents the interactions occurring within a vessel. The lower illustration the same events for a clot formed in a region of tissue damage.
This involves keeping thrombin in the damaged area. Most (85%) of the thrombin produced during clot formation remains attached to the fibrin threads and can not leave the region. This is represented by the dashed arrow with the 85% label--see both illustrations. Thrombin that escapes the clot (15%) is inactivated by antithrombin III as represented by the dashed arrow labeled 15% in both illustrations.
Antithrombin III is always present but its potency is increased 1000 times in the presence of heparin. Heparin is bound to the endothelium thus antithrombin III is always potent in blood vessels. However, in extravascular tissues, heparin is released (block arrow) from mast cells in the presence of components from damaged cells (stars) to increase the efficiency of antithrombin III.
The lysis (breakdown) of the fibrin mesh is accomplished by the enzyme plasmin as represented by the dashed arrow. The enzyme tissue plasminogen activator (TPA) converts plasminogen into plasmin as represented by the heavy arrow. TPA is secreted (block arrow) by the endothelium (top illustration) in the presence of thrombin (solid arrow).
In extravascular regions (bottom illustration) TPA is released when cells are damaged; it is only one of many compounds released (stars). As within blood vessels, plasminogen is converted to plasmin which begins dissolving the fibrin fibers in the clot (dashed arrow).
Last update: 7/19/2005