Platelets, platelets, in fresh human blood have the appearance of small colorless bodies of a round, oval or fusiform shape 2-4 microns in size. They can combine (agglutinate) into small or large groups (Fig. 4.29). Their quantity in human blood ranges from 2.0×10 9 /l to 4.0×10 9 /l. Platelets are non-nuclear fragments of the cytoplasm, separated from megakaryocytes - giant cells of the bone marrow.

Platelets in the bloodstream have the shape of a biconvex disc. When staining blood smears with azure-eosin, platelets reveal a lighter peripheral part - hyalomere and a darker, granular part - granulomere, the structure and color of which may vary depending on the stage of development of platelets. In the platelet population, there are both younger and more differentiated and aging forms. The hyalomere in young plates turns blue (basophilen), and in mature plates it turns pink (oxyphylene). Young forms of platelets are larger than old ones.

There are 5 main types of platelets in the platelet population:

1) young - with a blue (basophilic) hyalomere and single azurophilic granules in a reddish-violet granulomere (1-5%);

2) mature - with a slightly pink (oxyphilic) hyalomere and well-developed azurophilic granularity in the granulomere (88%);

3) old ones - with darker hyalomere and granulomere (4%);

4) degenerative - with a grayish-blue hyalomere and a dense dark purple granulomere (up to 2%);

5) giant shapes irritation - with a pinkish-purple hyalomere and purple granulomere, 4-6 microns in size (2%).

In diseases, the ratio of different forms of platelets may change, which is taken into account when making a diagnosis. An increase in the number of young forms is observed in newborns. In oncological diseases, the number of old platelets increases.

The plasmalemma has a thick layer of glycocalyx (15-20 nm), forms invaginations with outgoing tubules, also covered with glycocalyx. The plasma membrane contains glycoproteins that function as surface receptors involved in the processes of adhesion and aggregation of platelets.

The cytoskeleton in platelets is well developed and is represented by actin microfilaments and bundles (10-15 each) of microtubules arranged circularly in the hyolomere and adjacent to the inner part of the plasmolemma (Fig. 46-48). Elements of the cytoskeleton maintain the shape of platelets, participate in the formation of their processes. Actin filaments are involved in the reduction of the volume (retraction) of the formed blood clots.

There are two systems of tubules and tubules in the platelets, which are clearly visible in the hyalomere with electron microscopy. The first is an open system of canals associated, as already noted, with invaginations of the plasmolemma. Through this system, the contents of platelet granules are released into the plasma and absorption of substances occurs. The second is the so-called dense tubular system, which is represented by groups of tubes with electron-dense amorphous material. It resembles a smooth endoplasmic reticulum, formed in the Golgi apparatus. The dense tubular system is the site of the synthesis of cyclooxygenase and prostaglandins. In addition, these tubules selectively bind divalent cations and act as a reservoir of Ca 2+ ions. The above substances are essential components of the blood coagulation process.

Rice. 4.30. Platelets. A - platelets in a peripheral blood smear. B - diagram of the structure of a platelet. B - TEM. D - non-activated (marked with an arrow) and activated (marked with two arrows) platelets, SEM. D - platelets adhering to the wall of the aorta in the area of ​​damage to the endothelial layer (D, D - according to Yu.A. Rovenskikh). 1 - microtubules; 2 - mitochondria; 3 – u-granules; 4 - a system of dense tubules; 5 - microfilaments; 6 - system of tubules associated with the surface; 7 - glycocalyx; 8 - dense bodies; 9 - cytoplasmic reticulum.

The release of Ca 2+ from the tubules into the cytosol is necessary to ensure the functioning of platelets (adhesion, aggregation, etc.).

Organelles, inclusions and special granules were found in the granulomere. Organelles are represented by ribosomes (in young plates), elements of the endoplasmic reticulum, the Golgi apparatus, mitochondria, lysosomes, peroxisomes. There are inclusions of glycogen and ferritin in the form of small granules.

Special granules in the amount of 60-120 make up the main part of the granulomer and are represented by two main types - alpha and delta granules.

First type: a-granules- these are the largest (300-500 nm) granules with a fine-grained central part separated from the surrounding membrane by a small light space. They contain various proteins and glycoproteins involved in blood coagulation processes, growth factors, hydrolytic enzymes.

The most important proteins secreted during platelet activation include platelet factor 4, p-thromboglobin, von Willebrand factor, fibrinogen, growth factors (platelet PDGF, transforming TGFp), coagulation factor - thromboplastin; glycoproteins include fibronectin, thrombospondin, which play an important role in the processes of platelet adhesion. Heparin-binding proteins (thinning the blood, preventing blood clotting) include factor 4 and p-thromboglobulin.

The second type of granules - δ-granules(delta-granules) - represented by dense bodies 250-300 nm in size, in which there is an eccentrically located dense core surrounded by a membrane. There is a well-defined light space between the crypts. The main components of the granules are serotonin, accumulated from plasma, and other biogenic amines (histamine, adrenaline), Ca 2+ , ADP, ATP in high concentrations.

In addition, there is a third type of small granules (200-250 nm), represented by lysosomes (sometimes called A-granules) containing lysosomal enzymes, as well as microperoxisomes containing the enzyme peroxidase. The contents of the granules upon activation of the plates are released according to open system channels associated with the plasma membrane.

The main function of platelets is participation in the process of blood clotting - a protective reaction of the body to damage and preventing blood loss. Platelets contain about 12 factors involved in blood clotting. When the vessel wall is damaged, the plates quickly aggregate, stick to the resulting fibrin threads, resulting in the formation of a thrombus that closes the wound. In the process of thrombosis, several stages are observed with the participation of many components of the blood.

An important function of platelets is their participation in the metabolism of serotonin. Platelets are practically the only elements of the blood in which reserves of serotonin accumulate from plasma. Platelet binding of serotonin occurs with the help of high-molecular factors of blood plasma and divalent cations.

In the process of blood coagulation, serotonin is released from collapsing platelets, which acts on vascular permeability and contraction of vascular smooth muscle cells. Serotonin and its metabolic products have antitumor and radioprotective effects. Inhibition of serotonin binding by platelets was found in a number of blood diseases - malignant anemia, thrombocytopenic purpura, myelosis, etc.

The lifespan of platelets is an average of 9-10 days. Aging platelets are phagocytosed by spleen macrophages. Strengthening the destructive function of the spleen can cause a significant decrease in the number of platelets in the blood (thrombocytopenia). To eliminate this, an operation is required - the removal of the spleen (splenectomy).

With a decrease in the number of platelets, for example, with blood loss, thrombopoietin accumulates in the blood - a glycoprotein that stimulates the formation of plates from bone marrow megakaryocytes.

blood platelets

blood platelets, or platelets, in fresh human blood they look like small colorless bodies of a rounded or fusiform shape. They can combine (agglutinate) into small or large groups. Their number ranges from 200 to 400 x 10 9 in 1 liter of blood. Platelets are non-nuclear fragments of the cytoplasm, separated from megakaryocytes- giant cells in the bone marrow.

Platelets in the bloodstream have the shape of a biconvex disc. They reveal a lighter peripheral part - hyalomere and the darker, grainy part - granulomer. The platelet population contains both younger and more differentiated and aging forms. The hyalomere in young plates turns blue (basophilen), and in mature plates it turns pink (oxyphylene). Young forms of platelets are larger than old ones.

The platelet plasmalemma has a thick layer of glycocalyx, forms invaginations with outgoing tubules, also covered with glycocalyx. The plasma membrane contains glycoproteins that act as surface receptors involved in the processes of adhesion and aggregation of platelets (i.e., the processes of coagulation, or coagulation, of blood).

The cytoskeleton in platelets is well developed and is represented by actin microfilaments and bundles of microtubules arranged circularly in the hyalomere and adjacent to the inner part of the plasmolemma. Elements of the cytoskeleton maintain the shape of platelets, participate in the formation of their processes. Actin filaments are involved in the reduction of the volume (retraction) of the formed blood clots.

There are two systems of tubules and tubules in platelets. The first is an open system of channels associated, as already noted, with invaginations of the plasmalemma. Through this system, the contents of platelet granules are released into the plasma and absorption of substances occurs. The second is the so-called dense tubular system, which is represented by groups of tubules resembling a smooth endoplasmic reticulum. The dense tubular system is the site of the synthesis of cyclooxygenase and prostaglandins. In addition, these tubules selectively bind divalent cations and act as a reservoir of Ca2+ ions. The above substances are essential components of the blood coagulation process.

The release of Ca 2+ ions from the tubules into the cytosol is necessary to ensure the functioning of platelets. Enzyme cyclooxygenase metabolizes arachidonic acid to form prostaglandins and thromboxane A2, which are secreted from the laminae and stimulate their aggregation during blood coagulation.

With the blockade of cyclooxygenase (for example, acetylsalicylic acid), platelet aggregation is inhibited, which is used to prevent the formation of blood clots.

Organelles, inclusions and special granules were found in the granulomere. Organelles are represented by ribosomes, elements of the endoplasmic reticulum of the Golgi apparatus, mitochondria, lysosomes, peroxisomes. There are inclusions of glycogen and ferritin in the form of small granules.

Special granules make up the bulk of the granulomer and come in three types.

The first type is large alpha granules. They contain various proteins and glycoproteins involved in blood coagulation processes, growth factors, and lytic enzymes.

The second type of granules are delta granules containing serotonin accumulated from plasma and other biogenic amines (histamine, adrenaline), Ca2+ ions, ADP, ATP in high concentrations.

The third type of small granules, represented by lysosomes containing lysosomal enzymes, as well as microperoxisomes containing the enzyme peroxidase.

The contents of the granules upon activation of the plates are released through an open system of channels associated with the plasmalemma.

The main function of platelets is participation in the clotting process, or coagulation, of blood - a protective reaction of the body to damage and preventing blood loss. Platelets contain about 12 factors involved in blood clotting. When the vessel wall is damaged, the plates quickly aggregate, stick to the resulting fibrin threads, resulting in the formation of a thrombus that covers the defect. In the process of thrombosis, several stages are observed with the participation of many components of the blood.

At the first stage, there is an accumulation of platelets and the release of physiologically active substances. At the second stage - the actual coagulation and stop bleeding (hemostasis). First, active thromboplastin is formed from platelets (the so-called internal factor) and from the tissues of the vessel (the so-called external factor). Then, under the influence of thromboplastin, active thrombin is formed from inactive prothrombin. Further, under the influence of thrombin, fibrinogen is formed fibrin. All these phases of blood coagulation require Ca2+.

Finally, on last third stage, retraction of the blood clot is observed, associated with the contraction of actin filaments in the processes of platelets and fibrin filaments.

Thus, morphologically, at the first stage, platelet adhesion occurs on the basement membrane and on the collagen fibers of the damaged vascular wall, as a result of which platelet processes are formed and granules containing thromboplastin emerge from the plates through the tubule system. It activates the conversion of prothrombin to thrombin, and the latter affects the formation of fibrin from fibrinogen.

An important function of platelets is their participation in metabolism. serotonin. Platelets are practically the only blood elements in which serotonin reserves accumulate from plasma. Platelet binding of serotonin occurs with the help of high-molecular factors of blood plasma and divalent cations with the participation of ATP.

In the process of blood coagulation, serotonin is released from collapsing platelets, which acts on vascular permeability and contraction of vascular smooth muscle cells.

The lifespan of platelets is an average of 9-10 days. Aging platelets are phagocytosed by spleen macrophages. Strengthening the destructive function of the spleen can cause a significant decrease in the number of platelets in the blood (thrombocytopenia). This may require removal of the spleen (splenectomy).

With a decrease in the number of platelets, for example, with blood loss, the blood accumulates thrombopoietin- a factor that stimulates the formation of plates from bone marrow megakaryocytes.

· hemophilia- a hereditary disease caused by a deficiency of factors VIII or IX of blood coagulation; manifested by symptoms of increased bleeding; inherited in a recessive sex-linked type;

· purpura- multiple small hemorrhages in the skin and mucous membranes;

· thrombocytopenic purpura- the general name of a group of diseases characterized by thrombocytopenia and manifested by hemorrhagic syndrome (eg, Werlhof's disease);

Part Four - Blood formula, leukocyte formula, age-related changes in blood, lymph characteristics.

Hemogram and leukogram

In medical practice, blood analysis plays a huge role. In clinical tests, the chemical composition of the blood (including the electrolyte composition) is examined, the amount of formed elements, hemoglobin, erythrocyte resistance, erythrocyte sedimentation rate and many other indicators are determined. In a healthy person, the formed elements of the blood are in certain quantitative ratios, which are usually called a hemogram, or a blood formula.

The so-called differential count of leukocytes is important for characterizing the state of the body. Certain percentages of leukocytes are called leukogram, or leukocyte formula.

Age-related changes in blood

The number of erythrocytes at the time of birth and in the first hours of life is higher than in an adult, and reaches 6.0-7.0 x 10 12 in 1 liter of blood. By 10-14 days it is equal to the same figures as in an adult organism. In subsequent periods, there is a decrease in the number of erythrocytes with minimal indicators at the 3-6th month of life (the so-called physiological anemia). The number of red blood cells returns to normal values ​​during puberty. Newborns are characterized by the presence of anisocytosis with a predominance of macrocytes, an increased content of reticulocytes, as well as the presence of a small number of nucleated erythrocyte precursors.

The number of leukocytes in newborns is increased and reaches 30 x 10 9 in 1 liter of blood. Within 2 weeks after birth, their number drops to 9-15 x 10 9 in 1 liter (the so-called physiological leukopenia). By the age of 14-15, the number of leukocytes reaches the level that remains in an adult.

The ratio of the number of neutrophils and lymphocytes in newborns is the same as in adults 4.5-9.0 x 10 9 . In subsequent periods, the content of lymphocytes increases, and neutrophils decreases, and by the fourth or fifth day, the number of these types of leukocytes is equalized - this is the so-called. first physiological decussation leukocytes. A further increase in the number of lymphocytes and a drop in neutrophils lead to the fact that in the 1st-2nd year of a child's life, lymphocytes make up 65%, and neutrophils - 25%. A new decrease in the number of lymphocytes and an increase in neutrophils lead to the alignment of both indicators in 4-year-old children (this is the second physiological crossover). A gradual decrease in the content of lymphocytes and an increase in neutrophils continue until puberty, when the number of these types of leukocytes reaches the adult norm.

Lymph

Lymph is a slightly yellowish liquid tissue that flows in the lymphatic capillaries and vessels. It consists of lymphoplasm (plasma lymphae) and shaped elements. By chemical composition lymphoplasm is close to blood plasma, but contains less proteins. The lymphoplasm also contains neutral fats, simple sugars, salts (NaCl, Na2CO3, etc.), as well as various compounds, which include calcium, magnesium, and iron.

Formed elements of lymph are represented mainly by lymphocytes(98%), as well as monocytes and other types of leukocytes. Lymph is filtered from the tissue fluid into the blind lymphatic capillaries, where, under the influence of various factors, various components of the lymphoplasm constantly enter from the tissues. From the capillaries, the lymph moves to the peripheral lymphatic vessels, along them to the lymph nodes, then to the large lymphatic vessels and flows into the blood.

The composition of the lymph is constantly changing. There are peripheral lymph (i.e. to the lymph nodes), intermediate (after passing through the lymph nodes) and central (lymph of the thoracic and right lymphatic ducts). The process of lymph formation is closely related to the flow of water and other substances from the blood into the intercellular spaces and the formation of tissue fluid.

Some terms from practical medicine:

· neonatal jaundice, physiological - transient jaundice (hyperbilirubinemia), which occurs in most healthy newborns in the first days of life;

Thrombocytopathies can be hereditary (primary) and symptomatic (secondary).

Primary platelet dysfunction, which causes the development of hemorrhagic diathesis, is based on the following: main pathogenetic factors:

o defects in the surface membrane associated with the absence or blockade of receptors on the platelet membrane that interact with stimulators (agonists) of their adhesion and aggregation (Glantzmann's thrombasthenia, autosomal recessive deficiency of GP IIβ / IIIα, Bernard-Soulier thrombodystrophy, autosomal recessive deficiency of GP Iβ, combined with an increase in the size of platelets);

o violation of degranulation (release reaction) of platelets;

o deficiency of aggregation stimulators in platelet granules:

o diseases of the absence of dense granules (X-linked Wiskott-Aldrich syndrome, autosomal recessive Hermansky-Pudlak, Chediak-Higashi syndromes associated with deficiency of ADP, ATP, Ca 2+, etc.);

o diseases of the absence of α-granules (syndrome of "gray" platelets associated with a deficiency of fibrinogen, platelet factor 4, growth factor, etc.);

o deficiency, decreased activity and structural anomaly (violation of multidimensionality) of the von Willebrand factor. An example is von Willebrand's disease, usually inherited in an autosomal dominant manner, which is characterized by impaired platelet adhesion and ristomycin aggregation.

Primary violations of platelet aggregation can also be mediated by blockade of the formation of cyclic prostaglandins and TxA 2, the mobilization of calcium ions from the tubular system of platelets.

Acquired thrombocytopathies include tumor processes, including leukemia, DIC, liver and kidney diseases, vitamin B 12 and C deficiency, exposure to ionizing radiation, etc. special group secondary thrombocytopathies emit iatrogenic (drug) thrombocytopathies caused by a number of medicinal effects, some of which (aspirin, etc.) block the formation of powerful cyclic prostaglandin aggregation stimulators in platelets, in particular TxA 2, others block IIβ / IIIα receptors (thienopyridines, etc.) , others disrupt the transport of calcium ions into platelets or stimulate the formation of cAMP.

Mechanism of vascular-platelet hemostasis

Activation of vascular-platelet (primary) hemostasis causes a complete stop of bleeding from capillaries and venules and a temporary stop of bleeding from veins, arterioles and arteries by forming a primary hemostatic plug, on the basis of which, when secondary (coagulation) hemostasis is activated, a thrombus is formed.

Stages of vascular-platelet hemostasis:

Endothelial injury and primary vasospasm.

Microvessels respond to damage with a short-term spasm, as a result of which bleeding from them does not occur in the first 20-30 s. This vasoconstriction is determined capillaroscopically when an injection is made into the nail bed and is recorded by the initial delay in the appearance of the first drop of blood when the skin is punctured with a skin scarifier. It is caused by reflex vasospasm due to contraction of smooth muscle cells of the vascular wall and is supported by vasospastic agents secreted by the endothelium and platelets - serotonin, TxA 2, norepinephrine, etc.

Damage to the endothelium is accompanied by a decrease in thromboresistance of the vascular wall and exposure of the subendothelium, which contains collagen and expresses adhesive proteins - von Willebrand factor, fibronectin, thrombospondin.

2. Platelet adhesion to the site of deendothelialization.

It is carried out in the first seconds after damage to the endothelium through the forces of electrostatic attraction as a result of a decrease in the magnitude of the surface negative charge of the vascular wall in case of violation of its integrity, as well as platelet receptors for collagen (GP Ia / Pa), followed by stabilization of the formed connection by adhesion proteins - von Willebrand factor, fibronectin and thrombospondin, which form "bridges" between their complementary platelet GP and collagen.

Platelet activation and secondary vasospasm.

Activation is caused by thrombin, which is formed from prothrombin under the influence of tissue thromboplastin, FAT, ADP (released simultaneously with thromboplastin when the vascular wall is damaged), Ca 2+ , adrenaline. Platelet activation is a complex metabolic process associated with the chemical modification of platelet membranes and the induction of the glycosyltransferase enzyme in them, which interacts with a specific receptor on the collagen molecule and thereby ensures platelet “landing” on the subendothelium. Along with glycosyltransferase, other membrane-bound enzymes are activated, in particular phospholipase. A 2 , with the highest affinity for phosphatidylethanolamine. The hydrolysis of the latter triggers a cascade of reactions, including the release of arachidonic acid and the subsequent formation of short-lived prostaglandins (PGG 2, PGH 2) from it under the action of the cyclooxygenase enzyme, which are transformed under the influence of the thromboxane synthetase enzyme into one of the most powerful inducers of platelet aggregation and vasoconstrictors - TxA 2.

Prostaglandins contribute to the accumulation of cAMP in platelets, regulate phosphorylation and activation of the calmodulin protein, which transports Ca 2+ ions from the dense tubular system of platelets (equivalent to the sarcoplasmic reticulum of muscles) into the cytoplasm. As a result, the contractile proteins of the actomyosin complex are activated, which is accompanied by contraction of platelet microfilaments with the formation of pseudopodia. This further enhances platelet adhesion to the damaged endothelium. Along with this, due to Ca 2+ -induced contraction of microtubules, platelet granules are “pulled” to the plasma membrane, the membrane of depositing granules fuses with the wall of membrane-bound tubules, through which the granules are emptied. The reaction of the release of the components of the granules is carried out in two phases: the first phase is characterized by the release of the contents of dense granules, the second - α-granules.

TxA 2 and vasoactive substances released from dense platelet granules cause secondary vasospasm.

platelet aggregation.

TxA 2 and ADP, serotonin, β-thromboglobulin, platelet factor 4, fibrinogen, and other components of dense granules and α-granules released during platelet degranulation cause platelets to adhere to each other and to collagen. In addition, the appearance of PAF in the bloodstream (during the destruction of endotheliocytes) and components of platelet granules leads to the activation of intact platelets, their aggregation with each other and with the surface of platelets adhered to the endothelium.

Platelet aggregation does not develop in the absence of extracellular Ca 2+ , fibrinogen (causes irreversible platelet aggregation) and protein, the nature of which has not yet been elucidated. The latter, in particular, is absent in the blood plasma of patients with Glanzman's thrombasthenia.

The formation of a hemostatic plug.

As a result of platelet aggregation, a primary (temporary) hemostatic plug is formed that closes the vessel defect. Unlike a blood clot, a platelet aggregate does not contain fibrin filaments. Subsequently, plasma coagulation factors are adsorbed on the surface of the aggregate from platelets and the “internal cascade” of coagulation hemostasis is launched, culminating in the loss of stabilized fibrin filaments and the formation of a blood clot (thrombus) based on the platelet plug. With the reduction of thrombasthenin (from the Greek. stenoo- tighten, compress) platelet thrombus thickens (thrombus retraction). This is also facilitated by a decrease in the fibrinolytic activity of the blood responsible for the lysis of fibrin clots.

Along with the “internal cascade”, the “external cascade” of blood coagulation associated with the release of tissue thromboplastin is also included in the process of thrombosis. In addition, platelets can independently (in the absence of contact factors) trigger blood clotting by interacting with factor Va exposed on their surface with plasma factor Xa, which catalyzes the conversion of prothrombin to thrombin.

The classic scheme of blood coagulation according to Moravits (1905)

Interaction scheme coagulation factors

50. Platelets, development, structure, number and functional value.

Platelets, or platelets, have the appearance of small colorless bodies of a round, oval or fusiform shape 2-4 microns in size. They are combined into small or large groups. The number of platelets in human blood is 180-300 * 10 * 9 / l. They live from 8 to 11 days. Utilized in the spleen. Platelets are non-nuclear fragments of the cytoplasm, separated from megakaryocytes.In each platelet, 2 parts are distinguished:

Central - granulomer (darker, granular);

Peripheral - hyalomere (lighter part). The hyalomere in young plates turns blue, and in mature plates it turns pink.

In the population of platelets, 5 types of plates are distinguished: 1) young 1-5% 2) mature 88% 3) old 4% 4) degenerative 2% 5) giant forms of irritation (4-6 microns) 2%.

Young forms of platelets are larger than old ones.

Plasma membrane of plasma cells covered with a thick (15-20 nm) glycocalyx, forms invaginations in the form of tubules extending from the cytolemma. This is an open system of tubules through which their contents are released from platelets, and various substances come from blood plasma. The plasmalemma contains glycoprotein receptors. The PIb glycoprotein captures von Willebrand factor (vWF) from plasma. This is one of the main factors that ensure blood clotting. The second glycoprotein, PIIb-IIIa, is a fibrinogen receptor and is involved in platelet aggregation.

Hyalomer- The platelet cytoskeleton is represented by actin filaments located under the cytolemma, and bundles of microtubules adjacent to the cytolemma and located circularly. Actin filaments are involved in the reduction of thrombus volume.

Dense tubular system The platelet consists of tubules similar to smooth EPS. On the surface of this system, cyclooxygenases and prostaglandins are synthesized, divalent cations bind in these tubules and Ca 2+ ions are deposited. Calcium promotes adhesion and aggregation of platelets. Under the influence of cyclooxygenases, arachidonic acid breaks down into prostaglandins and thromboxane A-2, which stimulate platelet aggregation.

Granulometer includes organelles (ribosomes, lysosomes, microperoxisomes, mitochondria), organelle components (ER, Golgi complex), glycogen, ferritin and special granules.

Special granules are represented by the following 3 types:

1st type- alpha granules, have a diameter of 350-500 nm, contain proteins (thromboplastin), glycoproteins (thrombospondin, fibronectin), growth factor and lytic enzymes (cathepsin).

2nd type - beta granules, have a diameter of 250-300 nm, are dense bodies, contain serotonin from the blood plasma, histamine, adrenaline, calcium, ADP, ATP.

3rd type- granules with a diameter of 200-250 nm, represented by lysosomes containing lysosomal enzymes, and microperoxisomes containing peroxidase.

Platelet Functions:

Participate in the formation of blood clots when blood vessels are damaged. When a thrombus is formed, the following occurs: 1) the release of an external blood coagulation factor and platelet adhesion by tissues; 2) platelet aggregation and release of internal blood coagulation factor and 3) under the influence of thromboplastin, prothrombin turns into thrombin, under the influence of which fibrinogen falls into fibrin filaments and a thrombus is formed, which, by clogging the vessel, stops bleeding. When aspirin is injected into the bodythrombosis is suppressed.

Participate in the metabolism of serotonin. These are practically the only elements of the blood in which reserves of serotonin accumulate from plasma. Platelet binding of serotonin occurs with the help of high-molecular factors of blood plasma and divalent cations with the participation of ATP.

With a decrease in the number of platelets in the blood, thrombopoietin accumulates - GP, which stimulates the formation of plates from bone marrow megakaryocytes.

Platelets are free-circulating in the blood non-nuclear fragments of the cytoplasm of the giant cells of the red bone marrow - megakaryocytes. The size of platelets is 2-3 microns, their number in the blood is 200-300x10 9 liters. Each plate in a light microscope consists of two parts: a chromomere, or granulomere (intensely colored part), and a hyalomer (transparent part). The chromomere is located in the center of the platelet and contains granules, remnants of organelles (mitochondria, EPS), as well as inclusions of glycogen.

Granules are divided into four types.

1. a-granules contain fibrinogen, fibropectin, a number of blood coagulation factors, growth factors, thrombospondin (an analogue of the actomyosin complex, is involved in platelet adhesion and aggregation) and other proteins. Stained with azure, giving granulomere basophilia.

2. The second type of granules is called dense bodies, or 5-granules. They contain serotonin, histamine (incoming to platelets from plasma), ATP, ADP, calcine, phosphorus, ADP causes platelet aggregation in case of damage to the vessel wall and bleeding. Serotonin stimulates the contraction of the wall of the damaged blood vessel, and also first activates and then inhibits platelet aggregation.

3. λ-granules are typical lysosomes. Their enzymes are released when the vessel is injured and destroy the remnants of unresolved cells for better attachment of the thrombus, and also participate in the dissolution of the latter.

4. Microperoxisomes contain peroxidase. Their number is small.

In addition to granules, there are two systems of tubules in the platelet: 1) tubules associated with the cell surface. These tubules are involved in granule exocytosis and endocytosis. 2) a system of dense tubules. It is formed due to the activity of the Golgi complex of a megakaryocyte.

Rice. Diagram of platelet ultrastructure:

AG - Golgi apparatus, G - A-granules, Gl - glycogen. GMT - granular microtubules, PCM - ring of peripheral microtubules, PM - plasma membrane, SMF - submembrane microfilaments, PTS - dense tubular system, PT - dense bodies, LVS - superficial vacuolar system, PS - near-membrane layer of acidic glycosaminoglycans. M - mitochondria (according to White).

Functions of platelets.

1. Participate in blood clotting and stop bleeding. Platelet activation is caused by ADP secreted by the damaged vascular wall, as well as adrenaline, collagen and a number of mediators of granulocytes, endotheliocytes, monocytes, and mast cells. As a result of adhesion and aggregation of platelets during the formation of a thrombus, processes are formed on their surface, with which they stick together with each other. A white thrombus forms. Further, platelets secrete factors that convert prothrombin to thrombin, under the influence of thrombin, fibrinogen is converted to fibrin. As a result, fibrin strands form around the platelet conglomerates, which form the basis of a thrombus. Red blood cells are trapped in fibrin threads. This is how a red clot is formed. Platelet serotonin stimulates vessel contraction. In addition, due to the contractile protein thrombostenin, which stimulates the interaction of actin and myosin filaments, platelets closely approach each other, traction is also transmitted to fibrin filaments, the clot decreases in size and becomes impermeable to blood (thrombus retraction). All this helps to stop bleeding.

2. Platelets, simultaneously with the formation of a thrombus, stimulate the regeneration of damaged tissues.

3. Ensuring the normal functioning of the vascular wall, primarily the vascular endothelium.

There are five types of platelets in the blood: a) young; b) mature; c) old d) degenerative; d) gigantic. They differ in structure.

Lifespan

platelets is equal to 5-10 days. After that, they are phagocytosed by macrophages (mainly in the spleen and lungs). Normally, 2/3 of all platelets circulate in the blood, the rest are deposited in the red pulp of the spleen. Normally, a certain amount of platelets can go into the tissues (tissue platelets).

Impaired platelet function can manifest itself in both hypocoagulation and hypercoagulation of the blood. In the nervous case, this leads to increased bleeding and is observed in thrombocytopenia and thrombocytopathy. Hypercoagulability is manifested by thrombosis - the closure of the lumen of blood vessels in organs by thrombi, which leads to necrosis and death of part of the organ.