When a blood vessel is injured a number of physiological mechanisms are activated that promote hemostasis (hemo = blood; stasis = standing). Breakage of a blood vessel exposes collagen proteins to the blood. This initiates three separate, but over lapping hemostatic mechanisms - (1) vasoconstriction (2) the formation of a platelet plug, and (3) the production of a web of fibrin proteins (blood clot)
(1) Vasoconstriction: When a blood vessel is damaged, the smooth muscles in it's wall contract, which makes the lumen of the vessels narrow, sometimes so strongly that blood flow is completely stopped.
(2) Platelet-plug formation: When the endothelium is ruptured, platelets adhere to the collagen and release some secretions. These secretions aggregate other platelets and make them sticky, so that they adhere to those already stuck on the collagen and form a 'platelet- plug'.
(3) Production of web of fibrin protein: The third mechanism for hemostasis is the formation of clot. The activator substances from the injured vascular wall, platelets and blood proteins adhering to the injured vascular wall, initiate the clotting process. Clot is a web of fibrin with blood cells trapped in it.
Mechanism of blood clotting
Clotting of blood takes place in three essential steps.
i) Step -1: It involves the formation of a complex of activated substances collectively called as the prothrombin activator. It is formed by a complex cascade of chemical reactions that occur in the blood by the involvement of clotting factors in two pathways.
(a) Intrinsic pathway: It occurs when the blood is exposed to collagen
of injured wall of blood vessel in This activates of the Factor XII and in turn it by the activates another clotting factor that which activates yet another reaction [cascade fashion), which results in the formation of the
prothrombin activator.
(b) Extrinsic pathway: It occurs when the damaged vascular wall or extra vascular tissue comes into contact with blood. This activates the release of the tissue thromboplastin from the damaged tissue. It activates the FacEor VU.'IAS a result of these cascade reactions, the final product formed is the prothrombin activator.
ii) Step -2: The prothrombin activator, in the presence of sufficient amounts of ionic Ca++, causes the conversion of inactive prothrombin to active thrombin (activation of prothrombin).
iii) Step -3: Thrombin converts the soluble protein fibrinogen into soluble fibrin monomers which are been held together by the weak hydrogen bonds. The fibrin stabilizing by the factor (Factor XIII released from platelets) replaces hydrogen bonds with covalent bonds and cross links the fibres to form a 'mesh work. The insoluble mesh work of fibrin fibers spreading in all directions adhere to the damaged surfaces and trap the blood cells and platelets.
Within a few minutes after the clot is formed. It begins to contract so that the fluid is expelled out. This is called clot retraction and the fluid thus formed is the serum [plasma without fibrinogen).
