Introduction
Platelets or thrombocytes are the smallest figurative elements of the blood, with a discoidal shape and a diameter between 2 and 3 µm. Unlike white blood cells (or leukocytes) and red blood cells (or erythrocytes), platelets are not real cells, but cytoplasmic fragments of megakaryocytes located in the red marrow. These, in turn, derive from precursors called megakaryblasts and appear as large multinucleated cells (diameter 20 to 15 nm), which after various stages of maturation undergo phenomena of cytoplasmic fragmentation, originating from 2000 to 4000 platelets. Thrombocytes, therefore, have no nucleus (like red blood cells) and structures such as the endoplasmic reticulum and the Golgi apparatus; they are however delimited by a membrane, which makes each platelet independent of the others, and possess granules, various cytoplasmic organelles and RNA.
As anticipated, the dimensions of the plates are particularly contained; despite this their internal structure is extremely complex, since they intervene in a primary biological process called haemostasis [ haima, blood + stasis block]. In synergy with the coagulation enzymes, the platelets allow the passage of blood from the fluid to the solid state, forming a kind of cork (or thrombus) that obstructs the injured spots of the vessels.
Normal blood values
In one milliliter of blood, 150, 000 to 400, 000 platelets are normally present. Their average life is 10 days (against 120 of red blood cells), at the end of which they are swallowed up or destroyed by macrophages, especially in the liver and spleen (in the latter there is about one third of the total platelet mass). Every day between 30, 000 and 40, 000 platelets are produced per mm3; if necessary, this summary can increase 8 times.
Platelet structure
The structure of the platelets is extremely complex, so that they are activated only in response to precise and well-defined stimuli; if this were not the case, platelet aggregation in circumstances that are not strictly necessary, or a defect in need, would have very serious consequences for the organism (pathological thrombogenesis and hemorrhage).
Since an incorrect blood coagulation plays a role of primary importance in the genesis of strokes and cardiac infarcts, the biological mechanisms that control it are still the subject of numerous studies.
Platelets are always present in the circulation, but they are activated only when there is damage to the walls of the circulatory system.
The structure of the platelets, as well as their shape and volume, change profoundly in relation to the degree and the stage of activity. In the inactive form, the platelets are made up of a paler part (ialomer) and a more refractive central part (chromomer), rich in granules containing coagulation proteins and cytokines. The cell membrane is rich in protein molecules and glycoproteins, which act as receptors by regulating the interaction of platelets with the surrounding environment (adhesion and aggregation).
Coagulation and platelets
Platelets are just some of the many actors involved in the coagulation process. Following the lesion of a blood vessel, the release of some chemicals by endothelial cells, and the exposure of the collagen of the damaged wall, determine the activation of platelets (the endothelium is a particular lining of the inner surface of blood vessels, which in normal conditions separates the fibers of the collagen matrix from the blood preventing platelet adhesion).
The platelets rapidly adhere to the collagen exposed in the damaged wall (platelet adhesion) and are activated by releasing specific substances (called cytokines) in the area of the lesion. These factors promote the activation and association of other platelets, which aggregate to form a fragile stopper, the so-called white thrombus; moreover, they contribute to reinforce the local vasoconstriction previously triggered by some paracrine substances, released by the injured endothelium with the aim of decreasing blood flow and pressure. Both reactions are mediated by the release of substances contained within some platelet granules, such as serotonin, calcium, ADP and platelet activating factor (PAF). The latter triggers a signaling pathway that converts the phospholipids of the platelet membrane into thromboxane A2, which has a vasoconstrictor action and promotes platelet aggregation.
Platelets are extremely fragile: a few seconds after the lesion of a vessel they aggregate and break, releasing the contents of their granules into the blood and favoring the formation of the clot.
The aggregation of thrombocytes must obviously be limited to prevent the platelet plug from spreading into areas not affected by endothelial damage; platelet adhesion to healthy vessel walls is thus limited by the release of NO and prostacyclin (an eicosanoid).
The primary platelet plug is consolidated in the next phase, in which a series of reactions follow one another rapidly
While prostacyclin released by healthy endothelial cells inhibits platelet adhesion, our body synthesizes anticoagulants - such as heparin, antithrombin III and protein C - to block and regulate certain reactions involved in the coagulation cascade, which must necessarily be confined to the injured area.
| PHASES OF THE HEMOSTASIS PROCESS |
Vascular phase → reduction of vascular lumen Contraction of the vascular musculature Peripheral vasoconstriction Platelet phase → formation of the platelet plug adhesion Change of form degranulation Aggregation Coagulation phase → fibrin clot formation: Enzymatic reaction cascade Fibrinolytic phase → clot dissolution: Activation of the fibrinolytic system |
Platelets have an essential role in stopping bleeding, but they do not intervene directly in the repair of the damaged vessel, which is instead due to cell growth and division processes (fibroblasts and smooth vascular muscle cells). Once the leak has been repaired the clot dissolves slowly and retracts due to the action of the enzyme plasmin trapped inside the clot.
Pistrine and blood analysis
- PLT: platelet count, number of platelets per blood volume
- MPV: mean platelet volume
- PDW: amplitude of distribution of platelet volumes (index of platelet anisocytosis)
- PCT: or platelet hematocrit, volume of blood occupied by pistrine
