Blood clotting

There are two processes protective nature, cooperating with each other:

    1) blood clotting, blood loss warning of injury of blood vessels, resulting in the formation of blood clot – thrombus occluding the place injured, and 2) Anti warning blood clots, creates an obstacle to blood flow, and provides blood flow through the vessels.
Blood coagulation

When wound of the blood vessel at the site of its discontinuity platelets are easily broken, which leads to the exit of these vasoconstrictive substances – serotonin and blood coagulation. Studying the process of blood coagulation is important for the prevention of fatal bleeding and to preserve the blood used in transfusions it.

The thrombus occludes the place and prevents further injury blood loss. It consists of the insoluble protein filaments – fibrin – and formed elements, mainly erythrocytes. Therefore, a blood clot is red. But if, releasing blood to stir her wand, then settle on a stick strands of fibrin. After washing, these filaments can be seen that the fibrin light yellow, almost white. Human blood begins to clot in 3-4 minutes, 5-12 minutes, the clot formed. After coagulation of blood loss is accelerating.

Blood clotting – enzymatic process (A. Schmidt). There are three interrelated phase of blood coagulation:

    1) formation of thromboplastin, 2) the formation of thrombin, 3) the formation of fibrin. If blood coagulation occurs hemostasis – stop the bleeding. Hemostasis – a very complex process, involving many factors (or substances) contained in platelets, designated by Arabic numerals and existing or formed in the plasma, designated by Roman numerals.

With the destruction of platelets released more than a dozen factors. The most studied are:

    1) activates prothrombin in the presence of thromboplastin and calcium. Its action is identical to the factor V plasma. 2) accelerates the conversion of fibrinogen to fibrin by the action of thrombin. It is assumed that it blocks the effect of inhibitors (absorbers are) the formation of fibrin. 3) a phospholipid, formed in dependence on the function of the spleen and has no species specificity. Participates in the formation of thromboplastin activates it and regulates the plasma factor VII and IX. 4) neutralizes antithrombin effect of heparin and its influence on the formation of thromboplastin. 5) fibrinogen, located on or within the platelets. 6) inhibits the breakdown of fibrin, or fibrinolysis.

The plasma formed or have the following factors involved in clotting (procoagulants). Almost all of them are globulins. I – fibrinogen – globulin protein is synthesized in the liver. II – inactive enzyme prothrombin. In plasma, there are two types of prothrombin: active, turning into thrombin, and inactive, is not converted into thrombin. The composition comprises prothrombin nitrogen 18 amino acids (methionine, lysine, tryptophan, cystine, etc.), Carbohydrates and sulfur. The average plasma contains about 10 mg% of prothrombin, is synthesized in the liver with the obligatory participation of vitamin K. Vitamin K deficiency delayed its synthesis. III – enzyme thromboplastin. It fosfolipoproteid. There antitromboplastin. IV – calcium ions. V – aktselerator (accelerator) – globulin plasma. The action of thrombin proaktselerin inactive go active accelerin serum. It is synthesized in the liver. There he inhibitor. VI – aktselerator – globulin serum. In human factors V and VI have species specific. Both factors are identical. VII – proconvertin. When coagulation is converted to the active form – Convertino. Participates in the conversion of prothrombin to thrombin and in the formation of tissue thromboplastin. VIII – antigemofilichesky globulin A. Participates in the formation of thromboplastin, and possibly thrombin. When coagulation is destroyed, so it is not in the serum. In men whose blood is greater than in women. There he inhibitor. IX – plasma thromboplastin component (factor of Christmas). Participates in the formation of thromboplastin time, activated by damaged blood vessel. Its content is reduced by a lack of vitamin K. There is an inhibitor of it. X – protein trombotropin. It participates in the formation of plasma thromboplastin. XI – the precursor of plasma thromboplastin (PTA). Participates in the formation of thromboplastin activates factor VIII. XII – contact factor (Hageman). It is activated on contact with the damaged vessel wall. In plasma, it is inactive due to the action on it of the inhibitor. XIII – fibrinostabiliziruyuschy factor retarding the dissolution of fibrin. In plasma it is inactive and is activated by thrombin in the presence of calcium ions.

With the participation of factors platelet and plasma coagulation occurs as follows:
Phase 1 – the most difficult, during which formed thromboplastin – complex complex compound having the enzymatic activity. Distinguish blood (plasma) and tissue thromboplastin. Education plasma thromboplastin begins with the contact of blood with blood vessel damage and destruction of platelets. It involves platelet factor 3 and plasma factors IV, V, VIII, IX, X, XI and XII. Tissue thromboplastin is formed with tissue damage. It involves tissue extract, plasma factors IV, V, VII and X.

Phase 2 is characterized in that under the action of thromboplastin (blood or tissue) from a prothrombin to thrombin is formed. First, there is a small amount of thrombin by reacting plasma factors IV, VII and X, platelet factor 1 and prothrombin. Then, thrombin activates factor V, which dramatically speeds up its further education. Thrombin – glyukoproteidov.
3rd phase – the formation of fibrin from fibrinogen. It involves thrombin, fibrinogen, calcium ions and factors of 2 and 4 platelet. Fibrinogen – globulin, dissolved in plasma. It is converted into the insoluble protein fibrin in two phases. Phase enzyme, wherein the precursor is formed in the blood of fibrin – profibrin or fibrin monomer. The second phase physicochemical – fibrin monomer polymerizes and turns into fibrin which is insoluble under the action of fibrin-stabilizing factor XIII.

Vitamin K is necessary for the synthesis of prothrombin trombotropina (factor X) and factor VII.

After the formation of a blood clot within a few hours it is reduced and it is forced from whey – clot retraction. The platelets contain retraktin enhancing retraction. After retraction, with the participation of the enzyme fibrinolizina (plasmin) fibrin split. In plasma, the enzyme is in inactive form in the form of plasminogen (Plasminogen) relating to globulins. The plasma and platelets contain inhibitor fibrinolizina – serozyme.

Pain, cold and heat, and the sudden change of environment reflex accelerate clotting. The sympathetic nervous system and adrenaline influence mainly on the blood clotting, and the parasympathetic system and acetylcholine – to protivosvertyvanie.
Stimulation of the sympathetic nervous system and the flow of blood and adrenaline accelerate clotting. The middle part of the reticular formation of the hypothalamic region accelerates and lateral part of it slows down clotting. The stop bleeding involved sympathetic and parasympathetic system, and after stopping the predominant role of the parasympathetic system, which prevents further increase in clot, as it promotes the appearance of anticoagulant factors. It is proved that direct stimulation of the cerebral cortex accelerates blood clotting.

Upon excitation of brain neurons accelerates blood clotting, and when braking – is slowing.

Hormones of the posterior lobe of the pituitary gland, as well as one of its hormones of the anterior lobe (STH), hormones cortical and medullary layers of the adrenal glands, the male sex hormone (testosterone), the female sex hormone (progesterone) accelerate blood clotting and thyroid hormone – slows down.

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Blood clotting