Chapter 2. Physiology

Physiology in numbers Newton managed to express the movement of celestial bodies in mathematical equations. Mathematical thought has the power to transform biology, pathology and medicine. In its most basic application it can facilitate the discovery of new possibilities for

Physiology of muscles There are three types of muscles: striated skeletal muscles, striated cardiac muscle and smooth muscles. Muscles have the following physiological properties: 1. excitability, i.e. the ability to be excited by the action of stimuli; 2.

Physiology of synapses The term “synapse” was introduced by C. Sherrington. A synapse is a functional connection between a nerve cell and other cells. Synapses are those areas where nerve impulses can influence the activity of a postsynaptic cell, exciting or

Physiology of the heart

Physiology of sleep Sleep is a physiological state that is characterized by the loss of active mental connections of the subject with the world around him. Sleep is vital for higher animals and humans. For a long time it was believed that sleep represents rest,

Color index (CPU), or farb index (Fi), is a relative value that gives an idea of ​​the hemoglobin (Hb) content in an individual red blood cell (E) compared to the standard.

The standard is calculated as follows. The hemoglobin content in one red blood cell is equal to the quotient of the amount of Hb divided by the number of red blood cells. CP = Hb g/l*3 / 2 first digits of red blood cell count*10. Normally, the color index ranges from 0.75-1.0 and very rarely can reach 1.1. In this case, the red blood cells are called normochromic.

The color index is used in clinical practice for the differential diagnosis of anemia. Most anemias are accompanied hypochromia (a decrease in the amount of Hb in an erythrocyte), the color index will be less than 0.75. Hypochromia occurs as a result of a decrease in either the size of erythrocytes or the amount of hemoglobin (with anemia caused by blood loss, infection, etc.) Hyperchromia observed in pernicious anemia, severe anemia in children, CP in these cases will be more than 1.1. Hyperchromia depends solely on an increase in the size of red blood cells.

4. The first phase of blood coagulation, external and internal cycles (the main factors involved in the formation of prothrombinase).Blood clotting process is predominantly a proenzyme-enzyme cascade in which proenzymes, passing into an active state, acquire the ability to activate other blood coagulation factors. Such activation can be sequential and retrograde.

The process of blood coagulation can be divided into three phases: the first includes a set of sequential reactions leading to the formation of prothrombinase, in the second phase the transition of prothrombin (factor II) to thrombin (factor IIa) occurs, and in the third phase fibrin is formed from fibrinogen.

First phase - the formation of prothrombinase can occur by external and internal mechanisms. The external mechanism requires the presence of thromboplastin (factor III), while the internal mechanism is associated with the participation of platelets (factor P3) or destroyed red blood cells. At the same time, the internal and external pathways of prothrombinase formation have much in common, since they are activated by the same factors (factor XIIa, kallikrein, VMC, etc.), and also ultimately lead to the appearance of the same active enzyme - factor Xa , performing the functions of prothrombinase. In this case, both complete and partial thromboplastin serve as matrices on which enzymatic reactions unfold in the presence of Ca2+ ions.

The formation of prothrombinase along the external pathway begins with the activation of factor VII during its interaction with thromboplastin and factor XIIa. In addition, factor VII can become active under the influence of factors XIa, IXa, Xa, IIa and kallikrein. In turn, factor VIIa not only converts factor X to Xa (leading to the appearance of prothrombinase), but also activates factor IX, which is involved in the formation of prothrombinase by an internal mechanism.

The formation of prothrombinase through the external pathway occurs extremely quickly (in 20-30 s), leads to the appearance of small portions of thrombin (IIa), which promotes irreversible platelet aggregation, activation of factors VIII and V and significantly accelerates the formation of prothrombinase through the internal mechanism. The initiator of the internal mechanism of prothrombinase formation is factor XII, which is activated by the injured surface of the vessel wall, skin, collagen, adrenaline, in laboratory conditions - upon contact with glass, after which it converts factor XI to XIa. Kallikrein (activated by factor XIIa) and BMC (activated by kallikrein) may participate in this reaction. Factor XIa has a direct effect on factor IX, converting it to factor IXa. The specific activity of the latter is aimed at proteolysis of factor X and occurs with the obligatory participation of factor VIII (or VIIIa).

It should be noted that the activation of factor X under the influence of a complex of factors VIII and IXa is called the tenase reaction.

Ticket 5 1. Agglutigation reaction, conditions for its development. ABO blood groups. Agglutination - the process of gluing red blood cells, and it occurs only with certain combinations of serum and red blood cells.

Specific proteins in the red blood cell membrane - agglutinogens A and B, and in the blood plasma - specific proteins - agglutinins α and β. For each group according to the AB0 system, there is a certain combination of these proteins, two out of four:

Erythrocyte antigen system ABO. It is known that there are four blood groups. On what basis can the blood of all people on the planet be divided into only four blood groups? It turns out that based on the presence or absence of only two antigens in the erythrocyte membrane, A and B, four options the presence of these antigens on the erythrocyte membrane: option 1 - the erythrocyte membrane contains neither antigen A nor antigen B, such blood is classified as group I and is designated O(I). Option 2 - red blood cells contain only antigen A - the second group A (II). Option 3 - red blood cells contain only antigen B - the third group B (III). Option 4 - red blood cells contain both antigens - A and B - blood group AB (IV).

The intravascular conversion of fibrinogen to fibrin, which is normally very limited, can increase significantly during shock. Fibrinolysis is the main mechanism that ensures, under these conditions, the maintenance of the liquid state of the blood and the patency of blood vessels, primarily the microvasculature.

The fibrinolytic system includes plasmin and its precursor plasminogen, plasminogen activators, and inhibitors of plasmin and activators (Fig. 12.3). Fibrinolytic activity of the blood increases under various physiological conditions of the body (physical activity, psycho-emotional stress, etc.), which is explained by the entry of tissue plasminogen activators (tPA) into the blood. It can now be considered established that the main source of plasminogen activator found in the blood is the cells of the vascular wall, mainly the endothelium.

Although in vitro experiments have shown the release of tPA from the endothelium, the question remains whether such secretion is a physiological phenomenon or simply a consequence of “leakage”. Under physiological conditions, there appears to be very little release of tPA from the endothelium. With vessel occlusion and stress, this process intensifies. Biologically active substances play a role in its regulation: catecholamines, vasopressin, histamine; kinins increase, and IL-1, TNF and others decrease the production of tPA.

In the endothelium, along with tPA, its inhibitor, PAI-1 (plasminogen activator inhibitor-1), is also formed and secreted. PAI-1 is found in cells in greater quantities than tPA. In blood

									-FHP
		PAI-I- -
	PAI-II-

alpha2 Macroglobulin ------ *~Plasmin -

Fibrinogen

(D-fragment)

Rice. 12.3. Fibrinolytic system:

TPA - tissue plasminogen activator; PAI-I - tPA inhibitor; PAI-II - urokinase inhibitor; a Gir C - activated protein C; HMK - high molecular weight kininogen; FDF - degradation products of fibrin (fibrinogen); _ _ -

inhibition;----------- - activation

and subcellular matrix, PAI-1 is associated with the adhesive glycoprotein vitronectin. In this complex, the biological half-life of PAI-1 increases 2-4 times. Due to this, the concentration of PAI-1 in a certain region and local inhibition of fibrinolysis is possible. Some cytokines (IL-1, TNF) and endothelium suppress fibrinolytic activity mainly by increasing the synthesis and secretion of PAI-1. In septic shock, the content of PAI-1 in the blood is increased. Disruption of the participation of the endothelium in the regulation of fibrinolysis is an important link in the pathogenesis of shock. The detection of a large amount of tPA in the blood is not yet evidence of fibrinolysis occurring. Tissue plasminogen activator, like plasminogen itself, has a strong affinity for fibrin. When it is released into the blood, plasmin is not generated in the absence of fibrin. Plasminogen and tPA can coexist in the blood but do not interact. Plasminogen activation occurs on the surface of fibrin.

The activity of tPA present in human plasma disappears rapidly both in vivo and in vitro. The biological half-life of tPA released after administration of nicotinic acid to healthy people is 13 minutes in vivo and 78 minutes in vitro. The liver plays the main role in the elimination of tPA from the blood; with its functional insufficiency, a significant delay in elimination is observed. Inactivation of tPA in the blood also occurs under the influence of physiological inhibitors.

The formation of plasmin from plasminogen under the influence of tissue activators is considered as an external mechanism of activation.

plasminogen mutations. The internal mechanism is associated with the direct or indirect action of f. CN and kallikrein (see Fig. 12.3) and demonstrates the close relationship between the processes of blood coagulation and fibrinolysis.

An increase in blood fibrinolytic activity detected in vitro does not necessarily indicate activation of fibrinolysis in the body. Primary fibrinolysis, which develops with a massive intake of plasminogen activator into the blood, is characterized by hyperplasminemia, hypofibrinogenemia, the appearance of fibrinogen breakdown products, a decrease in plasminogen, plasmin inhibitors, and a decrease in blood f. Y and f. Yiii. Markers of fibrinolysis activation are peptides that are detected at an early stage of the action of plasmin on fibrinogen. With secondary fibrinolysis, which develops against the background of hypocoagulation, the content of plasminogen and plasmin in the blood is reduced, hypofibrinogenemia is sharply expressed, and a large number of fibrin degradation products (FDP) are detected.

A change in fibrinolytic activity is observed in all types of shock and has a phase character: a short-term period of increase in fibrinolytic activity and its subsequent decrease. In some cases, usually with severe shock, secondary fibrinolysis develops against the background of DIC.

The most pronounced primary fibrinolysis is observed during shock from electrical trauma, which is used for therapeutic purposes in a psychiatric clinic and develops mainly when current passes through the brain. At the same time, the time of lysis of plasma euglobulins sharply decreases, which indicates the activation of fibrinolysis. At the same time, the shock that occurs when current passes through the chest is not accompanied by activation of fibrinolysis. It has been shown that these differences are explained not by different levels of plasminogen activator in the brain and heart, but by activation of fibrinolysis if the electric shock is accompanied by muscle cramps. Perhaps this causes compression of the veins by contracted muscles and release of plasminogen activator from the endothelium (Tyminski W. et al., 1970).

Experimental studies have shown that during electric shock, plasminogen activators are released not only from the vascular endothelium, but from the heart, the renal cortex and, to a lesser extent, the lungs and liver (Andreenko G.V., Podorolskaya L.V., 1987). In the mechanism of release of plasminogen activator during electric shock, neurohumoral stimulation is of primary importance. In traumatic shock, primary fibrinolysis is also often observed. Thus, already in the early stages after injury (1-3 hours), victims experience an increase in fibrinolytic activity (Pleshakov V.

L., Tsybulyak G.N., 1971; Suvalskaya L.A. et al., 1980). A certain role here may be played not only by the release of vascular and tissue plasminogen activators, but also by the activation of f. XII. One of the mechanisms for activation of fibrinolysis during traumatic shock is a decrease in the activity of the CI esterase inhibitor, which activates f. HPa and kallikrein. As a result, the duration of circulation of activators of internal fibrinolysis increases. The degree of activation of fibrinolysis may also depend on the location of the injury, since the content of plasminogen activator in different tissues is not the same.

The biological half-life of plasmin is about 0.1 s; it is very quickly inactivated by a2-antiplasmin, which forms a stable complex with the enzyme. This, apparently, can explain the fact that in a number of cases primary fibrinolysis is not detected in the initial period of traumatic shock and, moreover, suppression of fibrinolysis is observed. Thus, in case of trauma to the abdominal organs (stage II-III shock) against the background of hypercoagulation, the presence of soluble fibrin-monomer complexes in the blood, fibrinolytic activity was reduced (Trushkina T.V. et al., 1987). This may be due to a sharp increase in the production of plasmin inhibitors as a response to the initial short-term hyperplasminemia. Total antiplasmin activity increases primarily due to α2-antiplasmin, as well as plasminogen activator inhibitor and histidine-rich glycoprotein. This reaction was described in detail by I. A. Paramo et al. (1985) in patients in the postoperative period.

After the primary activation of fibrinolysis in trauma complicated by shock, a stage of decreased fibrinolytic activity and/or secondary fibrinolysis develops. With the rapid development of shock, DIC syndrome and secondary fibrinolysis develop very quickly (Deryabin I.I. et al., 1984).

In the mechanism of inhibition of fibrinolysis in shock, what is important is primarily an increase in general antiplasmin activity (mainly a2-antiplasmin), as well as a glycoprotein rich in histidine, which interferes with the binding of plasminogen to fibrin. Against the background of a decrease in fibrinolytic activity in the systemic circulation, local fibrinolysis in the damaged area appears to be enhanced. This is evidenced by the amount of PDF in the blood after injury.

Data on the fibrinolytic activity of blood during hemorrhagic shock are very contradictory, which is explained by differences in the volume of blood loss, associated complications, etc. (Shuteu Yu. et al., 1981; Bratus V.D., 1991). Experimental data also did not bring complete clarity to this issue. Thus, I. B. Kalmykova (1979) observed in dogs after blood loss (40-45% of the blood volume, blood pressure = 40 mm Hg) an increase in fibrinolysis against the background of hypercoagulation, and in the hypocoagulation phase fibrinolysis decreased. In similar experiments, within 3 hours after blood loss, R. Garsia-Barreno et al. (1978) found that the time of lysis of plasma euglobulins and fibrinogen concentration did not change, and after 6 hours some inhibition of fibrinolysis was observed.

It is fundamentally important that changes in fibrinolysis during hemorrhagic shock are secondary, i.e., they occur against the background of circulatory hypoxia, metabolic acidosis, etc. In other types of shock, activation of fibrinolysis can occur regardless of hemodynamic disturbances (for example, with electric shock).

In septic shock, fibrinolytic activity changes very quickly and, as with other types of shock, has a phase character: increased fibrinolysis, inhibition, secondary fibrinolysis (does not develop in all cases). R. Garcia-Barreno et al. (1978) tracked changes in the fibrinolytic activity of the blood in dogs with endotoxin shock, starting from the 30th minute and up to 6 hours after the release of Escherichia coli lipopolysaccharide. Fibrinolytic activity in experimental animals increased sharply, fibrinogen concentration decreased, and PDF was detected in 100% of animals after 1 hour. Consequently, coagulopathic changes, including fibrinolysis, developed independently of hemodynamic disorders, hypoxia, etc.

In the mechanism of activation of fibrinolysis during septic shock, the main importance is attached to the internal pathway of plasminogen activation with the participation of f. XII and kallikrein (see Fig. 12.3). Primary hyperfibrinolysis in endotoxin shock develops due to the interaction of endotoxin with the serum complement system through activation of the properdin system. Component C3 and the last components of complement (C5-C9) activate both fibrinolysis and hemocoagulation.

Given that septic shock causes rapid and severe endothelial damage, it is safe to assume the involvement of an extrinsic plasminogen activation mechanism. Finally, in patients with septic shock, a decrease in Cl-esterase inhibitor, which is an inhibitor of fibrinolysis, was detected - it inactivates f. CPA and kallikrein (Colucci M. et al.,

1985). At the same time, under the influence of endotoxin, the formation of a fast-acting inhibitor of plasminogen activator increases (Blauhut B. et al., 1985). The significance of this regulatory mechanism remains to be studied.

If during traumatic, septic, hemorrhagic shock and electric shock, most researchers identify the initial period of activation of fibrinolysis, then in the early phase of cardiogenic shock fibrinolytic activity is reduced, and in the late phase it is increased (Lyusov V. A. et al., 1976; Gritsyuk V. I. and al., 1987). This is probably explained by the fact that acute myocardial infarction, complicated by cardiogenic shock, develops against the background of significant changes in the hemostatic system - hypercoagulation, tension of the fibrinolytic system, etc. This leads to depletion of the reserves of the vascular plasminogen activator, therefore, in cardiogenic shock and Primary hyperfibrinolysis does not develop, despite severe hyperadrenalineemia. In the later stage of shock, hypofibrinogenelia, thrombocytopenia, and a decrease in f. activity are recorded. And, Y, YII, positive paracoagulation tests, i.e. signs of intravascular coagulation, and against this background secondary hyperfibrinolysis develops.

Changes in fibrinolytic activity during shock not only demonstrate a violation of the functional state of the hemostatic system, but also have pathogenetic significance. Increasing fibrinolysis in the initial stage of shock undoubtedly has a positive effect, since the dissolution of fibrin helps maintain the suspension stability of the blood and microcirculation. On the other hand, increased fibrinolysis against the background of a deficiency of procoagulants disrupts the coagulation mechanism of hemostasis. The breakdown products of fibrinogen and fibrin (FDP) have antithrombin, antipolymerase activity, inhibit platelet adhesion and aggregation, which reduces the effectiveness of platelet-vascular hemostasis. Thus, the pathogenetic significance of increased fibrinolysis during shock (especially secondary fibrinolysis) is that this increases the likelihood of hemorrhages.

Internal and external pathway of activation

Fibrinolysis scheme. Blue arrows - stimulation; red arrows - suppression

Fibrinolysis, like the process of blood coagulation, occurs via an external or internal mechanism. The external activation pathway is carried out with the integral participation of tissue activators, synthesized mainly in the vascular endothelium. These activators include tissue plasminogen activator (tPA) and urokinase.

The internal activation mechanism is carried out thanks to plasma activators and activators of blood cells - leukocytes, platelets and erythrocytes. The internal activation mechanism is divided into Hageman-dependent and Hageman-independent. Hageman-dependent fibrinolysis occurs under the influence of blood coagulation factor XIIa, kallikrein, which causes the conversion of plasminogen to plasmin. Hageman-independent fibrinolysis occurs most rapidly. Its main purpose is to cleanse the vascular bed of unstabilized fibrin, which is formed during the process of intravascular coagulation.

Fibrinolysis inhibition

The fibrinolytic activity of the blood is largely determined by the ratio of inhibitors and activators of the fibrinolysis process.

Regulation of fibrinolysis

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See what "Fibrinolysis" is in other dictionaries:

Fibrinolysis… Spelling dictionary-reference book

- (from fibrin and...lysis), dissolution of intravascular thrombi and extravascular fibrin clots under the influence of proteolytic. blood plasma enzymes and formed elements, primarily plasmin. Proteins that carry out phosphorus are an integral part of the anti... ... Biological encyclopedic dictionary

Noun, number of synonyms: 1 dissolution (14) ASIS Dictionary of Synonyms. V.N. Trishin. 2013… Synonym dictionary

- (fibrin + Greek lysis disintegration, decomposition) the process of dissolving a fibrin clot as a result of enzymatic reactions; with thrombosis f. leads to canalization of the blood clot... Large medical dictionary

- (from Fibrin and Greek lýsis - decomposition, dissolution) dissolution of intravascular blood clots and extravascular fibrin deposits under the action of the enzyme Fibrinolysin. It is important for maintaining the fluid state of the blood and patency... ... Great Soviet Encyclopedia

FIBRINOLYSIS- (fibrinolysis) the process of dissolving blood clots, including the breakdown of the insoluble protein fibrin under the action of the enzyme plasmin. The latter is present in the blood plasma in the form of a passive precursor (plasminogen), which is activated... ... Explanatory dictionary of medicine

fibrinolysis- fibrolysin... A short dictionary of anagrams

- (syn. fibrinogenolysis of cadaveric blood) F. blood of a corpse during sudden death, as a result of which such blood remains uncoagulated; the reasons for F. are unclear... Large medical dictionary

The process of dissolving blood clots, including the breakdown of the insoluble protein fibrin by the enzyme plasmin. The latter is present in the blood plasma in the form of a passive precursor (plasminogen), which is activated simultaneously with... ... Medical terms

fibrinolysin- fibrinolysis in, and ... Russian spelling dictionary

Books

• Pharmacology and pharmacotherapy (set of 2 books), Satoskar R.S. , Bandarkar S.D. , The first volume of the two-volume manual is devoted to general issues of pharmacology. It examines the routes of administration and biological action of medicinal substances, their metabolism and excretion, mechanism,… Category: Pharmacology, formulation Publisher: Medicine,
• Magazine “Attending Physician” No. 01/2015, Open systems, Magazine “Attending Physician” is a professional medical publication. News from the medical and pharmaceutical markets, scientific and practical articles for general practitioners, therapists, pediatricians,… Category: Medicine Series:

The term "fibrinolysis" refers to the process of dissolving a blood clot. During the coagulation process, fibrinolysis prevents disruption of microcirculation in regions of the body outside the damage zone, and after bleeding stops, recanalization of the thrombus and restoration of blood supply in tissues distal to the site of thrombus formation. the process of destruction (lysis) of a blood clot is associated with the breakdown of fibrin and fibrinogen by a system of enzymes, the active components of which are plasmin. Plasmin hydrolyzes fibrin, fibrinogen, factors V, VII, XII, prothrombin.

Plasmin in the blood is in an inactive state in the form of plasminogen and is activated by tissue and blood activators. Tissue plasminogen activators are synthesized by the vascular endothelium. The most important among them are tissue plasminogen activator (tPA) and urokinase, which is produced in the kidney by the juxtagiomerular apparatus.

The intrinsic activation pathway is divided into Hageman-dependent and Hageman-independent. Hageman-dependent is carried out by f XIIa, VMC and caplicrein. Hageman-independent proceeds through the mechanism of urgent reactions and is carried out by plasma proteinases. There are fibrinolysis inhibitors in plasma: a 2 - antiplasmin, C 1 and a 1 - protease inhibitors, a 2 - macroglobulin. The activators are: a specific activator from endothelial cells; activated factor XII when interacting with kallikrein and high molecular weight kininogen; urokinase, produced by the kidney; bacterial streptokinase.

A disruption of the blood coagulation process occurs when there is a deficiency or absence of any factor involved in homeostasis. For example, the hereditary disease hemophilia is known, which occurs only in men and is characterized by frequent and prolonged bleeding. This disease is caused by a deficiency of factors VIII and IX, which are called antihemophilic factors.

Blood clotting can occur under the influence of factors that accelerate and slow down this process.

Factors that accelerate the blood clotting process:

Destruction of blood cells and tissue cells (increases the output of factors involved in blood clotting);

Calcium ions (participate in all main phases of blood clotting);

Thrombin;

Vitamin K (participates in the synthesis of prothrombin);

Heat (blood clotting is an enzymatic process);

Adrenalin.

Under normal conditions, the blood in the vessels is always in a liquid state, although conditions for the formation of intravascular blood clots constantly exist. Maintaining the fluid state of blood is ensured by self-regulation mechanisms due to the existence of corresponding functional systems. The main links in maintaining the fluid state of blood are the coagulation and anticoagulation systems. Currently, it is customary to distinguish two anticoagulant systems - the first and the second.

The first anticoagulant system (PAC) neutralizes thrombin in the circulating blood provided that it is formed slowly and in small quantities. Neutralization of thrombin is carried out by anticoagulants, which are constantly in the blood and therefore the PPS functions constantly. Such substances include:

Fibrin, which adsorbs part of thrombin;

Antithrombins prevent the conversion of prothrombin to thrombin;

Heparin blocks the transition phase of prothrombin to thrombin and fibrinogen to fibrin, and also inhibits the first phase of blood coagulation;

Lysis products (destruction of fibrin), which have antithrombin activity, inhibit the formation of prothrombinase;

Cells of the reticuloendothelial system absorb thrombin from blood plasma.

With a rapid increase in the amount of thrombin in the blood, PPS cannot prevent the formation of intravascular thrombi. In this case, the second anticoagulant system (ACS) comes into play, which ensures the maintenance of the liquid state of blood in the vessels through a reflex-humoral pathway. A sharp increase in the concentration of thrombin in the circulating blood leads to irritation of vascular chemoreceptors. Impulses from them enter the giant cell nucleus of the reticular formation of the medulla oblongata, and then along the efferent pathways to the reticuloendothelial system (liver, lungs, etc.). Heparin and substances that carry out and stimulate fibrinolysis (for example, plasminogen activators) are released into the blood in large quantities.

Heparin inhibits the first three phases of blood coagulation and interacts with substances that take part in blood coagulation. The resulting complexes with thrombin, fibrinogen, adrenaline, serotonin, factor X11I, etc. have anticoagulant activity and a lytic effect on unstabilized fibrin.

Regulation of blood clotting.

Regulation of blood coagulation is carried out using neuro-humoral mechanisms. Excitation of the sympathetic department of the autonomic nervous system, which occurs during fear, pain, and stressful conditions, leads to a significant acceleration of blood clotting, which is called hypercoagulation. The main role in this mechanism belongs to adrenaline and norepinephrine. Adrenaline triggers a number of plasma and tissue reactions: the release of thromboplastin from the vascular wall, which quickly turns into tissue prothrombinase; adrenaline activates factor XII, which initiates the formation of blood prothrombinase; adrenaline activates tissue lipases, which break down fats and thereby increases the content of fatty acids in the blood, which have thromboplastic activity; adrenaline enhances the release of phospholipids from blood cells, especially from red blood cells.

Irritation of the vagus nerve or the administration of acetylcholine leads to the release of substances from the walls of blood vessels similar to those released under the action of adrenaline. Consequently, in the process of evolution, only one protective-adaptive reaction was formed in the hemocoagulation system - hypercoagulemia, aimed at urgently stopping bleeding. The identity of hemocoagulation shifts upon stimulation of the sympathetic and parasympathetic parts of the autonomic nervous system indicates that primary hypocoagulation does not exist, it is always secondary and develops after primary hypercoagulation as a result (consequence) of the consumption of part of the blood coagulation factors.

Acceleration of hemocoagulation causes increased fibrinolysis, which ensures the breakdown of excess fibrin. Activation of fibrinolysis is observed during physical work, emotions, and painful stimulation.

Blood coagulation is influenced by the higher parts of the central nervous system, including the cerebral cortex, which is confirmed by the possibility of changing hemocoagulation conditionally. It exerts its influence through the autonomic nervous system and endocrine glands, the hormones of which have a vasoactive effect. Impulses from the central nervous system arrive to the hematopoietic organs, to the organs that store blood and cause an increase in blood output from the liver, spleen, and activation of plasma factors. This leads to the rapid formation of prothrombinase. Then humoral mechanisms are turned on, which support and continue the activation of the coagulation system and at the same time reduce the effects of the anticoagulation system. The significance of conditioned reflex hypercoagulation appears to be in preparing the body to protect itself from blood loss.

The blood coagulation system is part of a larger system - the system for regulating the state of aggregation of blood and colloids (PACK), which maintains the constancy of the internal environment of the body and its state of aggregation at a level that is necessary for normal life by maintaining the fluid state of the blood and restoring the properties of the walls vessels that change even during their normal functioning. The blood coagulation system in the body is always in an active state, which is due to the continuous release of thromboplastin from naturally degrading cells. Hypercoagulation develops in states of pain and emotional stress, which occurs with activation of the sympathetic division of the autonomic nervous system. Catecholamines promote the release of thromboplastin from the walls. Adrenaline directly activates the Hageman factor and activates tissue lipases, which increases thromboplastic activity. Stimulation of the vagus nerve produces effects similar to those of adrenaline.