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Mechanisms of haemostasis
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Mechanisms of haemostasis

Vessel-thrombocytory (primary, microcirculatory).

Provides stoppage of bleeding in vessels of microcirculatory system with diameter less than 100 mkm. Vessel wall and thrombocytes take part in this mechanism. Results in white clot, which consists of thrombocytes.

2  Coagulatory (secondary, macrocirculatory). It is the continuation of vessel-thrombocytory and it is based on it. Provides stoppage of bleeding in vessels with diameter more than 100 mkm. Results in red clot, which consists of fibrin and formed blood elements.

The role of vessel wall in haemostasis

I Vessel wall participate activation of haemostasis with the help of following mechanisms:

Unmasking of the collagen

When blood vessel wall is damaged the collagen is unmasked. So it becomes available for the formed blood elements. Collagen provides contact activation of thrombocytes and Hageman’s factor (F. XII), which initiates the internal mechanism of blood coagulation.

Release of ADP

ADP is released from the damaged cells of vessel wall, and it is powerful activator of thrombocytes adhesion and aggregation.

Release of tissue thromboplastin

Thromboplastin is released from damaged cells of vessel wall and initiates external mechanism of blood clotting and formation of small amount of thromboplastin in the damaged place.

Release of Willebrant factor

Endotheliocytes of vessel wall form Willebrant factor – glycoprotein, which participates thrombocytes adhesion.

II Vessel wall provides maintenance of blood fluidity (thromboresistancy) with the help of following mechanisms:

Formation of prostacyclin. Prostacyclin is formed by endotheliocytes (derivative of arachidonic acid), which is powerful inhibitor of thrombocytes aggregation.

Formation of antithrombin III – powerful natural anticoagulant.

Ability of endothelium to fix heparin-antithrombin III complex on its surface, which increases activity of this complex in hundreds times.

Formation of fibrinolysis activators.

Endothelial Surface Factors. Probably the most important factors for preventing clotting in the normal vascular system are the smoothness of the endothelial cell surface, which prevents contact activation of the intrinsic clotting system; a layer of glycocalyx on the endothelium (glycocalyx is a mucopolysaccharide adsorbed to the surfaces of the endothelial cells), which repels clotting factors and platelets, thereby preventing activation of clotting; and a protein bound with the endothelial membrane, thrombomodulin, which binds thrombin. Not only does the binding of thrombin with thrombomodulin slow the clotting process by removing thrombin, but the thrombomodulin- thrombin complex also activates a plasma protein, protein C, that acts as an anticoagulant by inactivating activated Factors V and VIII.



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