Platelets have a specific morphological structure and biochemical composition, and have a relatively constant number in normal blood (for example, the number of human platelets is 0/0000 ~ 300000 per cubic millimeter/kloc), which plays an important role in the physiological and pathological processes such as hemostasis, wound healing, inflammatory reaction, thrombosis and organ transplant rejection.
Platelets exist only in the blood of mammals. In lower vertebrates, spindle cells play a role in blood coagulation, and fish begin to have specific platelets. Amphibians, reptiles and birds all have platelets in their blood. Platelets are spindle-shaped oval cells with nuclei, which are similar in function to platelets. Invertebrates have no specific platelets, such as mollusks, which have the functions of defense and wound healing. Crustaceans have only one kind of blood cells, which can also coagulate blood.
Platelet formation
Produced by megakaryocytes in hematopoietic tissue of bone marrow. Multifunctional hematopoietic stem cells differentiate directionally in hematopoietic tissue, forming primitive megakaryocytes and then becoming mature megakaryocytes. Many depressions are formed on the membrane surface of mature megakaryocytes, which extend into the cytoplasm. The cell membranes of adjacent depressions fuse with each other in the deep part of the depression, so that part of the cytoplasm of megakaryocyte is separated from the mother. Finally, these components separated from the cytoplasm of megakaryocyte surrounded by cell membrane leave megakaryocyte, enter blood circulation through blood sinus in bone marrow hematopoietic tissue and become platelets. The newly generated platelets first pass through the spleen, which stores about 1/3. The stored platelets can be freely exchanged with platelets entering the circulating blood to maintain the normal amount in the blood. The number of platelets produced by each megakaryocyte is about 200 ~ 8000 per cubic millimeter. It is generally believed that the production of platelets is regulated by thrombopoietin in blood, but its detailed process and mechanism are still unclear. The life span of platelets is about 7 ~ 14 days, which is about110 of the total platelets updated every day. Most aged platelets are taken from the spleen.
Morphogenesis
Normal platelets in circulating blood are concave, oval or disc-shaped, which are called circulating platelets. The average diameter of human platelets is about 2 ~ 4 microns, the thickness is 0.5 ~ 1.5 microns, and the average volume is 7 cubic microns. Although platelets have no nucleus, they have organelles, and in addition, there are scattered granular components inside. Once the platelets come into contact with the wound surface or the non-vascular intima surface such as glass, they expand rapidly, and the particles are concentrated towards the center. Many pseudopodes extend outward to become dendritic platelets, and most of the particles are released immediately, and the platelets fuse with each other to become viscous deformed platelets. Dendritic platelets can also become circulating platelets if their stimulating factors are eliminated in time, while viscous deformed platelets are irreversible. Platelets have complex structure and composition. Platelet membrane is a lipid membrane with protein bilayer attached or embedded, which contains a variety of glycoproteins. It is known that glycoprotein Ⅰ b is related to adhesion, glycoprotein Ⅱ b/Ⅲ a is related to aggregation, and glycoprotein ⅴ is the receptor of thrombin. The plasma layer (outer coating of platelets) composed of plasma protein, coagulation factors and molecules related to fibrinolysis system is attached to the platelet membrane. There are two kinds of pipeline systems in platelet cytoplasm: open pipeline system and dense pipeline system connected with the surface. The former is an intricate pipeline system formed by platelet membrane invagination in cytoplasm. Pipeline membrane and platelet membrane are continuous, and the inner surface of pipeline membrane also has the same outer coating as platelet membrane. Through this pipeline system, plasma can enter the interior of platelets, thus expanding the contact area between platelets and plasma. Because this developed pipeline system is connected with the surface, platelets form a sponge-like structure. The latter is a thin and short dense tube system, which is not connected with the outside world and is quite endoplasmic reticulum. There are more than ten layers of parallel microtubules under the platelet membrane around the platelet, and there are dense microfilaments (actin) and myosin near the platelet membrane, which are related to the maintenance of platelet morphology and deformation movement. There are two kinds of particles scattered in platelets: α particles and dense particles. The content of α particles is medium electron density, and some particles have nuclei with high electron density in the center. Alpha particles contain fibrinogen, platelet factor 4, cathepsin A, cathepsin D, acid hydrolase, etc. The contents of dense particles have extremely high electron density, and contain 5- hydroxytryptamine, ADP, ATP, calcium ion, adrenaline, antifibrinolytic enzyme, pyrophosphate and so on. In addition, there are mitochondria and glycogen particles in platelets.
physiological function
Thrombosis and Dissolution When blood vessels are injured, platelets are stimulated by activating factors at the injured site to form platelet clots, which mainly play a hemostatic role. Then platelets undergo complex changes to produce thrombin, which turns fibrinogen in the adjacent plasma into fibrin. Interlaced fibrin causes platelet clots and blood cells to entangle into blood clots, that is, thrombosis (see coagulation factor). At the same time, the platelet process extends into the fibrin network. With the contraction of platelet microfilaments (actin) and myosin, blood clots contract, and thrombus becomes more solid, which can stop bleeding more effectively. This is the second hemostasis. With the formation of thrombus, platelets release thromboxane A2; Dense particle and alpha particles release ADP, 5- hydroxytryptamine, platelet factor 4, beta-thromboglobulin, thrombin sensitive protein, cell growth factor, coagulation factor V, VII and vascular permeability factor through that pipeline system connecte with the surface, and these active substances have some functions by activating peripheral platelet, promoting vascular contraction and promoting fibrin formation. Substance can strengthen inflammation and immune response in the injured area.
When blood clots are formed in the injured parts of blood vessels and blood loss stops, it is necessary to prevent the blood clots from increasing indefinitely and avoid the resulting blood vessel blockage. At this time, 5- hydroxytryptamine produced by platelets acts on vascular endothelial cells to release plasminogen activator, promote the formation of plasmin, and then dissolve fibrin in thrombus. Platelets themselves also have plasminogen activator and plasminogen, which produce plasmin to participate in fibrinolysis during thrombosis.
It plays a role in the repair of vascular endothelial cells.
The rapid flow of blood in blood vessels sometimes damages the wall of blood vessels, and platelets can attach to the surface of endothelial cells from the flowing state, during which the cell membrane disappears and the cytoplasm fuses with each other, thus repairing endothelial cells.
Mechanisms of platelet adhesion, release and aggregation There are many different receptors on the platelet surface, which are activated by binding with corresponding ligands. When vascular endothelial cells are damaged, collagen types ⅰ and ⅲ in subcutaneous tissue are exposed, and there is an active site of 9-peptide structure. From this active site, the adhesion of platelets to the injured site was realized by VWF factor connecting with the receptor glycoprotein 1b on platelet membrane. After platelet activation, the annular microtubules are depressed inward. Platelets appear radial processes, in which microfilaments and microtubules consistent with their long axes appear. Particles are concentrated in the center of lamellae, close to the pipeline system connected with the surface. Platelets change from circulation to dendrite. Platelets seen on blood smear under optical microscope, such as divided into central granular area and peripheral transparent area, are the characteristics of this stage.
The adhered platelets begin to release their contents. With the change of platelet morphology, arachidonic acid in phospholipid molecules of platelet membrane lipid bilayer is released, and then thromboxane A2 is formed under the action of enzymes on platelet membrane. The release of platelet granule contents is not simultaneous. The reaction of releasing ADP and 5- hydroxytryptamine from dense particles appears rapidly. The release of α particles varies with its content sooner or later; Firstly, alpha particles containing platelet factor 4, beta thromboglobulin and other components are released, and then particles containing acid hydrolase (equivalent to lysosomes) are released. Release is a process that requires energy. The calcium pump on the membrane pumps Ca2+ into platelets and activates ATPase, which eventually leads to the contraction of platelets and the release of particles in platelets.
Adhesion between platelets is called aggregation. ADP, adrenaline, thrombin and collagen are all platelet aggregation agents. The aggregation process caused by different polymerization agents is different. If ADP is added, it can directly cause platelet aggregation, and ADP released by aggregated platelets can cause new platelet aggregation again. So that two aggregate waves can appear. Collagen itself can not directly cause platelet aggregation, but only after inducing platelets to release ADP. Up to now, the known aggregation mechanisms are arachidonic acid pathway, dense particle pathway and platelet activating factor pathway, and many factors such as Ca2+ and fibrinogen are known to be related to platelet aggregation. In activated platelets, arachidonic acid is released from platelet membrane, and finally thromboxane A2(TXA2) is formed under the action of different enzymes. Thromboxane A2 is the strongest polymerization agent known so far. Prostaglandin I2(PGI2) released by endothelial cells can increase the level of cyclic adenosine monophosphate (cAMP) and inhibit platelet aggregation by activating adenylate cyclase.
There are species differences in mammalian platelets. For example, rabbit platelet dense granules contain histamine in addition to serotonin, while human platelets do not respond to ADP and thrombin. Rabbits, rats, mice, pigs, sheep and horses did not respond to adrenaline. There are also species differences in 5- hydroxytryptamine content and reactivity to aggregation inhibitors.
With the development of biology and medicine, cell adhesion has become one of the important topics in cell biology. The study of platelet adhesion and aggregation is expected to make new progress in this subject, and platelets are also an ideal neuropharmacological model. The contraction and relaxation of platelets are similar to the activity of skeletal muscle.
How do platelets stop bleeding and accelerate coagulation?
When blood is injured and bleeding, there are many mechanisms of hemostasis and coagulation, but most of them are related to the role of platelets, which can be summarized as follows:
1. vasoconstriction helps to temporarily stop bleeding. Platelets can release vasoconstrictors such as 5- hydroxytryptamine and catechol, so that injured blood vessels can be closed to varying degrees, and the blood flow in the tubes can be reduced to prevent blood loss.
2. Form antithrombotic and block blood vessel rupture. Platelets are easy to adhere and deposit on the exposed collagen fibers of damaged blood vessels, and gather into groups to form antithrombotic; Thrombosis is directly plugged into the vascular fissure, which can not only block the blood vessel, but also maintain the integrity of the blood vessel wall.
3. Release substances that promote blood coagulation and accelerate the formation of blood clots at blood vessel rupture. In the process of producing some factors and starting endogenous and exogenous coagulation systems, injured blood vessels or tissues complete a series of enzymatic biochemical chain reactions in a few minutes under the comprehensive action of different factors released by platelets, which eventually leads to the transformation of soluble fibrinogen in plasma into insoluble fibrin. The molecular weight of fibrinogen is about 340,000. Under the electron microscope, several peptide chains form a spiral coiled four-stage structure, which looks like a cluster as a whole. Fibrin, on the other hand, is slender and filamentary, interwoven into a net, thus intercepting blood cells and forming jelly-like blood clots.
4. Release anti-fibrinolytic factor and inhibit the activity of fibrinolytic system. Fibrin in plasma is easily degraded by fibrinolytic system. Because platelets contain anti-fibrinolytic factors and inhibit the activity of fibrinolytic system, the formed blood clots will not collapse.
Platelets are the smallest blood cells in the blood. The blood cell count of normal people is100×109/l-300×109/l, accounting for 0.3% of blood volume. Women's menstrual period can be reduced by 50% ~ 75%, and the content of children is slightly lower. About 2/3 of platelets are in the peripheral blood circulation, and 1/3 is in the spleen. They exchange with each other.
Platelets are disc-shaped, ranging in diameter from 1 ~ 4 microns to 7 ~ 8 microns, with great individual differences (5 ~ 12 cubic microns). Platelets can move and deform, so they are polymorphic when observed by general methods. Platelet structure is complex, in short, it has three layers from the outside to the inside, that is, the periphery consisting of outer membrane, unit membrane and subfilm microfilament structure is 1 layer; The second layer is the gel layer, and microfilaments and microtubules parallel to the surroundings can be seen under the electron microscope. The third layer is the micro-organ layer, with mitochondria, dense bodies, residual nuclei and other structures.
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Reply: YC 153000- Jianghu Young Xia Level 7 6- 13 16: 17.
It is said in the book that red blood cells pass through capillaries in a single line, but when capillaries bleed, platelets will gush out to stop bleeding. Where do platelets come from?
I don't know if you have studied hard ~ ~ First of all, do you know the composition of blood ~ ~
Including platelets ~ ~ One-way passage in the book means that the capillary is just big enough for a red blood cell to pass through ~ and the red blood cell is very big in the blood (the biggest one you forget) ~ ~ The platelet is very small ~ ~ If it can be too small, of course it can pass through ~ ~ If it can pass through, it will naturally flow out of the circulating blood. Platelets in normal state are concave, oval or disc-shaped, which is called circulating platelets. The average diameter of human platelets is about 2 ~ 4 microns, the thickness is 0.5 ~ 1.5 microns, and the average volume is 7 cubic microns. Although platelets have no nucleus, they have organelles, and in addition, there are scattered granular components inside. Once the platelets come into contact with the wound surface or the non-vascular intima surface such as glass, they expand rapidly, and the particles are concentrated towards the center. Many pseudopodes extend outward to become dendritic platelets, and most of the particles are released immediately, and the platelets fuse with each other to become viscous deformed platelets. Dendritic platelets can also become circulating platelets if their stimulating factors are eliminated in time, while viscous deformed platelets are irreversible. Platelets have complex structure and composition. Platelet membrane is a lipid membrane with protein bilayer attached or embedded, which contains a variety of glycoproteins. It is known that glycoprotein Ⅰ b is related to adhesion, glycoprotein Ⅱ b/Ⅲ a is related to aggregation, and glycoprotein ⅴ is the receptor of thrombin. The plasma layer (outer coating of platelets) composed of plasma protein, coagulation factors and molecules related to fibrinolysis system is attached to the platelet membrane. There are two kinds of pipeline systems in platelet cytoplasm: open pipeline system and dense pipeline system connected with the surface. The former is an intricate pipeline system formed by platelet membrane invagination in cytoplasm. Pipeline membrane and platelet membrane are continuous, and the inner surface of pipeline membrane also has the same outer coating as platelet membrane. Through this pipeline system, plasma can enter the interior of platelets, thus expanding the contact area between platelets and plasma. Because this developed pipeline system is connected with the surface, platelets form a sponge-like structure. The latter is a thin and short dense tube system, which is not connected with the outside world and is quite endoplasmic reticulum. There are more than ten layers of parallel microtubules under the platelet membrane around the platelet, and there are dense microfilaments (actin) and myosin near the platelet membrane, which are related to the maintenance of platelet morphology and deformation movement. There are two kinds of particles scattered in platelets: α particles and dense particles. The content of α particles is medium electron density, and some particles have nuclei with high electron density in the center. Alpha particles contain fibrinogen, platelet factor 4, cathepsin A, cathepsin D, acid hydrolase, etc. The contents of dense particles have extremely high electron density, and contain 5- hydroxytryptamine, ADP, ATP, calcium ion, adrenaline, antifibrinolytic enzyme, pyrophosphate and so on. In addition, there are mitochondria and glycogen particles in platelets.
Blood already contains platelets, which are synthesized when bone marrow makes blood. It's just that they gather around the wound to stop the blood loss.
PS: Although red blood cells pass through capillaries in a single row, they also have blood, but the blood volume is small. As long as there is blood, there are platelets, because platelets are also part of blood. In other words, there are platelets in the capillaries, yes, there are.