Coagulation OR Clotting Of Blood
Circulatory System of Class 11
The mechanism which results in sealing off of a leaking or severed blood vessel to stop bleeding is called hemostatic mechanism. A leakage in a blood vessel inside the body is plugged or sealed by blood
platelets which adhere together to pile up into a sticky plug called thrombus. This process is called agglutination of the platelets.
Sometimes, a thrombus is so large as to block the bloodstream in the concerned vessel or capillary. This may prove fatal if it happens in such organs as brain, lungs, heart, etc.
Bleeding in tissue spaces or at body surface due to damage to a blood vessel is stopped by a different process called blood coagulation or clotting.
As described by Howell, this process is a complex series of sequential changes which can be grouped into three major steps as follows:
(i) First step: As a blood vessel or certain capillaries are torn at the site of an injury and bleeding starts, the platelets adhere to the damaged tissues and release a phospholipid, called platelet factor-3.
Traumatized tissues at the injury also relase a lipoprotein factor called thromboplastin. These two factors combine with calcium ions (Ca++) and certain proteins of the blood plasma to form an enzyme named prothrombinase.
(ii) Second step: In presence of Ca++, the prothrombinase inactivates an anticoagulant of blood called heparin or antiprothrombin. Heparin normally keeps the blood in ‘sol’ condition for its easy flow in the blood vessels. When heparin is inactivated, the prothrombinase easily catalyzes breakdown of an inactive plasma protein, prothrombin, into an active protein called thrombin and some small peptide chains.
(iii) Third step: Lastly, the thrombin, acting as an enzyme, first brings about depolymerization of a soluble plasma protein, the fibrinogen, into its monomers. Later, it stimulates repolymerization of these monomers into long, insoluble, fibre-like polymers of a different protein called fibrin. The thin, long and solid fibres or fibrin form a dense network upon the wound. Blood corpuscles become entrapped in this network. Thus, a red clot format at the wound in about 2 to 8 minutes after injury. It stops further bleeding. Soonafter, the clot starts contracting and a pale yellow fluid, called serum, starts oozing out from it.
This serum is blood plasma minus the corpuscles and fibrinogen.
The prothrombin and fibrinogen of blood plasma are formed in liver with the help of vitamin K. Hence, deficiency, not only of these proteins, but also of vitamin K causes haemophilia in which blood clotting
takes so much time that the patient generally dies due to excessive bleeding. This is a genetic disease.