GTC Biotherapeutics (fka GTCB)

[jessellivermore]

ATIII and platelet adhesion................

As my earlier post re. Hemostasis; hemostasis means blood stopping. Primary hemostasis, platelet adhesion (clumping) and vessel constriction are the way the body stops bleeding. The clot comes later to form a more reliable seal. Fibrogen converting to fibrin is the final step in the coagulation cascade. This final step is facilitated by thrombin. For the coagulation cascade to proceed to a fibrin clot the flow in the area must be very slow. This is a built in safety feature to prevent the clot from extending into the rest of the circulation. ATIII acts at several levels in the cascade. One is to block the action of thrombin.

This study showed ATIII apparently decreased platelet adhesion
(so does asprin) to fibrinogen in low flow situations, ie in situations where it would have more time to interact. This action on the platelets might come about directly, or by possibly blocking another active agent which tended to increase platelet adhesiveness. The result would be deminished primary hemostasis, and probably benefit in situations where intra vascular thombosis is a risk such as coronary athersclerosis etc.
Because of the way the cascade works, the slower the flow is through an area the less it takes to trigger off clotting.