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Stages of aggregation
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Stages of aggregation

Initial aggregation. It is performed at the same time with adhesion. The main reason of it is ADP with not-thrombocytory origin, which is released from damaged cells.

Reverse aggregation. Aggregation, which can be stopped. The main reason of it is thrombocytory ADP, thromboxan A2, arachidonic acid.

Irreversible aggregation. Aggregation with the damage of thrombocytes and it cannot be stopped. The reason of it is thrombin.

Mechanism of aggregation

Aggregation is performed in two stages:

Stage 1 – stage of thrombocytes activation (fig. 5.1).

Aggregants increase thrombocyte membrane permeability to calcium. By the concentration gradient calcium enters thrombocytes. Its concentration increases in these cells. Calcium causes following effects in thrombocytes:

contraction of myofibrils, which leads to formation of processes;

increase of hydrolysis rate of ATP with the formation of ADP, which is aggregant;

release (secretion) of granules;

activation of phospholipase A2, which leads to formation of arachidonic acid and thromboxan A2.

 

Figure 5.1 – Mechanism of aggregations

Stage 2 – stage of thrombocytes conglutination.

There are two mechanisms of this stage:

formation of bridges between thrombocytes, which are formed with Ca2+ and ADP;

formation of bridges between thrombocytes, which are formed with plasma proteins. These proteins are aggregation co-factors of plasma. Fibrinogen, albumins, agrexons A and B.

  Release reaction – is the process of granules secretion in thrombocytes.

There 2 types of release reaction:

reaction of early release, which is performed during adhesion and initial aggregation. Granules of 1 and 2 type are released during this reaction;

reaction of late release, which is performed during irreversible aggregation. Granules of 3 and 4 type are released during this reaction.

  Thrombus consolidation – packing, retraction of thrombus in consequence of which it loses extra water and become hard. Contraction of thrombus is performed with the help of protein thrombostenin.

 

Basic Theory More than 50 important substances that cause or affect blood coagulation have been found in the blood and in the tissues—some that promote coagulation, called procoagulants, and others that inhibit coagulation, called anticoagulants.Whether blood will coagulate depends on the balance between these two groups of substances. In the blood stream, the anticoagulants normally predominate, so that the blood does not coagulate while it is circulating in the blood vessels. But when a vessel is ruptured, procoagulants from the area of tissue damage become “activated” and override the anticoagulants, and then a clot does develop.

It is the cascade of biochemical reactions, which result in the formation of fibrin. Plasma factors of coagulation participate coagulative haemostasis:

I – Fibrinogen;

II – Prothrombin;

III – Tissue thromboplastin. (tissue factor);

IV – Ca2+ ions;

V – Proaccelerin, Ac-globulin, labile factor;

VI – Active form of factor V (accelerin);

VII – Proconvertin, stable factor;

VIII – Antihaemophilic globulin, antihaemophilic factor A;

IX – Christmas’s factor, antihaemophilic factor B;

X – Stuart-Prauer’s factor, prothrombinase;

XI – Plasma antecessor of thromboplastin, antiheamophilic factor C;

XII – Hageman’s factor, contact factor;

XIII – Fibrinstabilizing factor, fibrinase.

All factors of coagulation can be divided into few groups:

substrate for the reaction – F. I (fibrinogen);

Ca2+ ions;

accelerants of reactions: F. V (proaccelerin), F. VIII (antihaemophilic globulin);

proteolytic enzymes: F. II, F. III, F. VII, F. IX, F. X, F. XI, F. XII.

Coagulative reactions are based on the reactions of hydrolysis, which are performed by proteolytic enzymes. Reactions occur in phospholipids of membranes of destroyed erythrocytes and thrombocytes. Factors of coagulation are fixed on membrane with the help of Ca2+ ions.

The main stages of blood coagulation are described by Moravic in 1905.

There are 3 stages of blood coagulation:

Stage 1 – formation of active prothrombinase.

 In response to rupture of the vessel or damage to the blood itself, a complex cascade of chemical reactions occurs in the blood involving more than a dozen blood coagulation factors. The net result is formation of a complex of activated substances collectively called prothrombin activator.

Stage 2 – formation of thrombin.

 The prothrombin activator catalyzes conversion of prothrombin into thrombin.

Stage 3 – formation of fibrin.

The thrombin acts as an enzyme to convert fibrinogen into fibrin fibers that enmesh platelets, blood cells, and plasma to form the clot itself.



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