General Considerations And Physiological Importance Of Normal Hemostasis To Man
A General Overview
Normal hemostasis can be considered under two headings, the vascular platelet mechanisms and the coagulation mechanism, which are closely interconnected in several ways. When injured, the blood vessel contracts and retracts in an attempt to close the wound. This is brought about by the intrinsic contractile elements in the vessel wall. The platelets adhere to and aggregate at the site of endothelial injury. Simultaneously, the coagulation proteins are sequentially activated to generate thrombin which converts fibrinogen into fibrin. Fibrin forms a mesh in which platelets and other formed elements of blood are entangled to form a clot which arrests blood loss. The platelets contract and the fibrin plus is drawn together more tightly to the vessels wall. Once the optimum amount of clot has been formed, further extension is arrested by the antithrombic substances and the fibrinolytic enzyme plasmin, which is generated locally. Plasmin helps in removing excess of fibrin by converting it into soluble fibrin degradation products (FDP).
Thus, it will be seen that normal hemostasis is a well balanced system brought about by the close interaction of the vascular platelet factor, coagulation and fibrinolysis. This can be achieved only in the presence of normal vessel walls, adequate number of functioning platelets, sufficient quantities of functional coagulation proteins, and a normal fibrinolytic mechanism.
The endothelium which lines the blood vessels synthesizes factor VIII-related von willebrand factor (VWF). Following endothelium, platelets bind to factor VIII-vWF polymers and collagen, and adhere to the surface to initiate the hemostatic process. The normal vascular endothelium also produces a prostaglandin PGI2 (Prostacyclin, epoprostenol) which has the opposite effect, i.e vasodilation, prevention of platelet aggregation, and inhibition of adenosine diphosphate (ADP) release.
Normal count is 150- 300,000/cmm. They are disc-shaped, non-nucleated from the megakaryocytes in the bone marrow under the influence of thrombopoietin, a controlling factor. Platelets have a lifespan of about 10 days. The megakaryocytes remain extravascularly on the sinusoids and liberate the platelets into the vessels. The platelets contain several substances held in the different organelles (surface membrane, tubules, granules and vacuoles). These take part in the platelet adhesion, aggregation, release reaction and they interact with coagulation factors.
Functions of platelets
Platelets adhere to exposed subendothelial structures. The adhesion takes place between the platelets and subendothelial factor VIII-vWF polymers and collagen. This leads to change of shape from discs to spiny spheres and release of their granules locally and into blood. Adenosine disphosphate which is a strong platelet aggregating agent released from dense granules causes more platelets to aggregate and join the platelet plug already formed. Thrombin, formed as a result of coagulation reaction, causes further aggregation of platelets, so also does the stress hormone epinephrine, which also constricts the arteries and arterioles. Adhesion to vessel wall and aggregation of platelets result in change in their membrane structure. Platelet fatty acid cyclo-oxygenase, which is an enzyme, converts arachidoni acid into the endoperoxides. A prostaglandin derivative thromboxane A2 is produced which potentiates the release of the contents of the granules. It also leads to further platelet aggregation and local vasoconstriction. Thromboxane A2 is hydrolysed non-enzymically into thromboxane B2 which is an inactive product.
In addition to these intrinsic mechanisms, platelets adsorb various coagulation factors on their surface and provide a surface for them to be activated.
© 2014 Funom Theophilus Makama