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Endothelial cell apoptosis disorder

As already noted, apoptosis is considered as active process cell death, which is morphologically different from necrosis.

It occurs both normally and against the background of various pathological processes.

It is believed that disruption of this process makes a significant contribution not only to the development of autoimmune diseases, but also plays a role in important role in pathogenesis vascular diseases human (atherosclerosis, antiphospholipid syndrome (AFS), systemic vasculitis, etc.).

A number of substances that play key roles in the development of inflammatory and autoimmune reactions also cause apoptosis of the vascular endothelium. It has been shown that the introduction lipopolysaccharides (LPS) experimental animals leads to massive death endothelial cells (EC) aorta. This phenomenon is considered as the most early manifestation apoptosis, which precedes DNA fragmentation and disruption of the integrity of the cell membrane.

It is known that when platelets are activated, exposure to PS leads to the initiation of blood clotting. Negatively charged phospholipids are involved in factor VIII and IXa-dependent activation of factor X on EC. Annex V completely inhibits this reaction.

Endothelial cells subjected to apoptosis are able to increase the rate of activation of factor X. At the same time, PS appears on their surface. In a similar way, there is an increase in the number of anionic phospholipid molecules on the monocyte membrane, which is accompanied by an increase in the activity of the prothrombinase complex.

According to a number of authors, endoxin-stimulated ECs and tissue factors produced by monocytes during the development of apoptosis of these cells have procoagulant activity. It is important to note that proinflammatory cytokines, endotoxins, hypoxia, and homocysteinemia suppress the activity of thrombomodulin and heparan sulfate on the endothelial surface. At the same time, they induce EC apoptosis.

All this indicates that disruption of the normal mechanisms of EC apoptosis may have important in the development of blood coagulation disorders in patients with systemic vasculitis, atherosclerotic vascular lesions and especially APS.

Recent studies have shown that plasma from patients with thrombotic thrombocytopenic purpura and hemolytic uremic syndrome induces apoptosis of microvascular endothelial cells derived from skin, kidney and brain.

This phenomenon was accompanied by the appearance of Fas (CD95), a molecule associated with apoptosis, on their membrane. In contrast, no similar changes were observed in pulmonary and hepatic microvascular endothelial cells. These data allow us to discuss the causes of rare vascular damage to the kidneys and lungs in these conditions, and possibly in some forms of vasculitis and antiphospholipid syndrome.

Impaired anticoagulant activity of endothelial cells

Normally, the vascular endothelium has powerful anticoagulant activity. Suppression of the blood clotting process occurs through several mechanisms.

Due to the presence on its surface: thrombomodulin and protein S, which promote the activation of protein C; heparan sulfate, which through activation of antithrombin III accelerates the formation of thrombin

Due to the synthesis of: tissue factor inhibitors that block the formation of the tissue factor complex - VIIa-Xa; Annexin V, which prevents the binding of coagulation factors; tissue plasminogen activator.

Under the influence of a variety of influences, including proinflammatory cytokines (IL-1, TNF-a), LPS, atherogenic substances (LP(a), homocysteine), hypoxia, hyperthermia, infections, autoantibodies and immune complexes (IR), ECs quickly lose their anticoagulant potential and enter a prothrombotic state (Fig. 3.1).

Rice. 3.1. Relationship between inflammation and hypercoagulability

Changes in the functional properties of EC during activation or apoptosis, disruption of the integrity of the endothelial layer and associated thrombotic and/or occlusive changes in blood vessels have great value in the pathogenesis of individual clinical syndromes(nephritis), as well as some forms of systemic vasculitis (hemorrhagic vasculitis, Takayasu arteritis, giant cell arteritis (GKA), Kawasaki disease, etc.).

Thus, according to J.D. Costing et al. (1992), in SLE, the target for aPL may be individual components of the coagulation cascade, such as protein C and protein S, expressed on the endothelial membrane. Antiphospholipid antibodies, like a-nDNA, can cross-bind with negatively charged epitopes of glycosaminoglycan, which is a major component of the nonthrombogenic lining layer of the vascular endothelium, and inhibit heparin-dependent activation of antithrombin III.

Low plasma concentrations total protein S was found in patients with Takayasu arteritis, leukocytoclastic and hemorrhagic vasculitis [A.A. Baranov et al., 1996; K.V.Salojin et al., 1996]. IN active phase systemic vasculitis, there is a decrease in endothelial production of tissue plasminogen activator.

At the same time, ECs begin to synthesize a number of procoagulant substances. These include tissue factors, factor V, PAF, von Willebrand factor, tissue plasminogen activator inhibitor. These substances are also involved in the pathogenesis of vasculitis.

Tissue plasminogen activator inhibitor

Impairment of the anticoagulant activity of endothelial cells in vasculitis can also be mediated through disruption of the fibrinolysis process.

It is known that normally the destruction of fibrin occurs with the participation of the proteolytic enzyme - plasmin, which in turn is obtained from plasminogen under the influence of urokinase or tissue plasminogen activator. Tissue plasminogen activator is most important for this process.

It is produced in ECs and released from them into the bloodstream. Its further metabolism occurs in three directions. Thus, one part of the tissue plasminogen activator is destroyed in liver cells, the other combines with fibrin deposits and activates plasminogen, and the third is irreversibly inactivated by its inhibitor. At a high concentration of the latter substance in the blood plasma, it undergoes rapid (less than 1) inactivation large number circulating tissue plasminogen activator.

As noted above, when systemic vasculitis amid high activity inflammatory process detected in blood plasma low level tissue plasminogen activator. In some cases, this occurs against the background of increased endothelial synthesis of its inhibitor. Moreover, these violations are recorded within long period time even in clinically inactive patients.

Von Willebrand factor and von Willebrand factor antigen

Many researchers have noted an increase in serum concentrations in systemic vasculitis. von Willebrand factor (FV) And von Willebrand factor antigen(FW:Ag)[A.A. Baranov et al., 1993; A.D. Woolf et al., 1987; B. Bliel et al., 1991; A.D.Blann, 1993].

However, it is currently unclear whether this phenomenon has any pathogenetic significance, or whether it only reflects the severity of endothelial dysfunction in these diseases.

Participation of VWF in the development of systemic vasculitis and vascular pathology in diffuse connective tissue diseases, apparently, is directly related to its biological role in the human body. It is known that VWF is involved in the adhesion of platelets to the subendothelium in the area of ​​vascular damage.

It mediates the connection between membrane glycoproteins of non-activated platelets (GPIb-IX) and subendothelial molecules (collagen types I and III and heparan sulfate); interacting with GPIIb/IIIa receptors, enhances platelet aggregation, and also promotes activation of factor VIII by thrombin.

In plasma, VWF:Ag is mainly represented by a pool synthesized by the endothelium, which normally circulates in the form of multimers, but along with it there is also a small amount of unusually large forms of this glycoprotein. The latter have the ability to bind more effectively to platelet receptors (GPIb-IX, GPIIb-IIIa). Plasma also contains substances that break down large forms FV:Ag to small ones, without affecting, however, its fraction located in the subendothelium.

It is believed that with the constant production of von Willebrand factor antigen by endothelial cells, it has normal structure. Stimulation of the endothelium (oxidative stress, mechanical injury, histamine, membrane attack complex of complement, etc.) is accompanied by both increased synthesis of this glycoprotein and its release from the components of the endothelial cytoplasm (Weibel-Palade bodies).

The latter store VWF:Ag multimers, which have high functional activity in relation to binding to membrane receptors of non-activated platelets and adhesion of the latter to the subendothelium.

Increased production of VWF:Ag was noted during infections, stimulation of EC with endotoxin and proinflammatory cytokines IL-1, IF-γ, TNF-α.

High concentration VWF:Ag was found in patients with Wegener's granulomatosis and GCA who have concomitant infections [T.V. Beketova et al., 1996; M.C.Cid et al., 1996]. The ability to induce its production in endothelial culture is possessed by IgG fractions isolated from the sera of patients with APS or containing a-nDNA with activity antibodies to endothelial cells(AEKA) .

The possible participation of the von Willebrand factor antigen in the development of systemic vasculitis is explained by the example of hemolytic-uremic syndrome and thrombotic thrombocytopenic purpura (TTP), in which an increase in the macromolecular form of this glycoprotein in the blood serum is considered as one of the main pathogenetic mechanisms of these diseases. In systemic vasculitis, production of similar substances by the endothelium has also been detected.

It is known that the main morphological changes in TTP and hemolytic-uremic syndrome are characterized by thrombotic vasculopathy. Segmental occlusions of arterioles, capillaries and venules by hyaline thrombi are observed. The most pronounced changes are observed in the brain, kidneys, heart, and spleen.

In the early stages of the disease, thrombi in arterioles and capillaries consist predominantly of platelets, without perivascular infiltration, in which immunohistochemical analysis reveals a large amount of VWF: Ag and some fibrinogen or fibrin.

In primary and secondary antiphospholipid syndrome, similar changes are observed in the kidneys [Z.S. Alekberova et al., 1995; N.L. Kozlovskaya et al., 1995; E.L. Nasonov et al., 1995; M.A. Byron et al., 1987], and in patients with SLE glomerular thrombi and fibrin deposition in nephritis have been described. Moreover, with this disease high level VWF: Serum Ag is clearly associated with kidney damage.

A similar clinical and laboratory relationship can be traced in some forms of vasculitis (Wegener's granulomatosis, polyarteritis nodosa (UP), hemorrhagic vasculitis) [A.A. Baranov et al., 1993]. It is possible that in these cases, changes in the renal microvessels may be mediated through mechanisms similar to those in hemolytic-uremic syndrome and TTP.

IN lately On the membranes of young erythrocytes, platelet-like receptors are open, with which multiforms of von Willebrand factor can interact. Similar structures are also found on endothelial membranes. Thus, reticulocytes and other juvenile forms of red blood cells can attach to endothelial cells through VWF multimers and then participate in thrombus formation.

It seems that at a certain circle pathological conditions increased level von Willebrand factor antigen can be considered not only as a marker of severe damage to the blood vessels of the skin and kidneys, but also take an active part in their development.

It is possible that the entry into the bloodstream of an excess amount of abnormal forms of VWF: Ag, which are capable of more effectively binding to the membrane receptors of platelets and erythrocytes, and then the formation of blood clots in microvessels, enhances the disturbances in blood rheology that already exist in some systemic vasculitis (cryoglobulins, circulating immune complexes (CEC)) and contribute to the further progression of ischemic changes in tissues.

It is important to note that with systemic vasculitis, as well as with systemic lupus erythematosus in the active phase of the disease, a high level of VWF:Ag is often combined with impaired fibrinolytic activity of the blood plasma.

Nasonov E.L., Baranov A.A., Shilkina N.P.

"Everyone hopes to live a long time, but no one wants to be old"
Jonathan Swift

"A person's health, as well as his age, is determined by the condition of his blood vessels"
Medical axiom

Endothelium is a single layer of flat cells lining inner surface circulatory and lymphatic vessels, as well as the cavities of the heart.

Until recently it was believed that main function endothelium is the polishing of blood vessels from the inside. And only at the end of the twentieth century, after the award in 1998. Nobel Prize in the field of medicine, it became clear that the main cause of arterial hypertension (popularly called hypertension) and other cardiovascular diseases is a pathology of the endothelium.

It is now that we are beginning to understand how important the role of this body is. Yes, exactly the organ, because the total weight of endothelial cells is 1.5-2 kg (like the liver!), and its surface area is equal to the area of ​​a football field. So what are the functions of the endothelium, this huge organ distributed throughout the territory human body?

There are 4 main functions of the endothelium:

1. Regulation of vascular tone – maintaining normal blood pressure (BP); constriction of blood vessels when it is necessary to limit blood flow (for example, in the cold to reduce heat loss), or their expansion - in an actively working organ (muscle, pancreas during production digestive enzymes, liver, brain, etc.) when it is necessary to increase its blood supply.
2. Network expansion and restoration blood vessels. This function of the endothelium ensures tissue growth and healing processes. It is the endothelial cells throughout the vascular system of the adult body that divide, move and create new vessels. For example, in some organ, after inflammation, part of the tissue dies. Phagocytes eat dead cells, and in the affected area, germinating endothelial cells form new capillaries, through which stem cells enter the tissue and partially restore the damaged organ. This is how all cells, including nerve cells, are restored. Nerve cells are restored! This is a proven fact. The problem is not how we get sick. What matters is how we recover! It's not years that age you, but illnesses!
3. Regulation of blood clotting. The endothelium prevents the formation of blood clots and activates the blood clotting process when a vessel is damaged.
4. The endothelium is actively involved in the process of local inflammation - a protective survival mechanism. If somewhere in the body, something foreign sometimes begins to rear its head, then it is the endothelium in this place that begins to pass protective antibodies and leukocytes from the blood through the vessel wall into the tissue.

The endothelium carries out these functions by producing and secreting a large number of biologically different active substances. But the main molecule produced by the endothelium is NO - nitric oxide. It was the discovery of the key role of NO in the regulation vascular tone(in other words, blood pressure) and the condition of blood vessels in general, was awarded the Nobel Prize in 1998. A properly functioning endothelium continuously produces NO, maintaining normal pressure in vessels. If the amount of NO decreases as a result of decreased endothelial cell production or degradation by reactive radicals, the vessels cannot dilate adequately and deliver more nutrients and oxygen to actively working organs.

NO is chemically unstable - it only exists for a few seconds. Therefore, NO acts only where it is released. And if somewhere the endothelial functions are impaired, then other, healthy endothelial cells cannot compensate for local endothelial dysfunction. Local insufficiency of blood supply develops - ischemic disease. Specific organ cells die and are replaced by connective tissue. Aging of organs develops, which sooner or later manifests itself as pain in the heart, constipation, dysfunction of the liver, pancreas, retina, etc. These processes occur slowly, and often unnoticed by the person himself, but they accelerate sharply with any disease. The more severe the disease, the more massive the tissue damage, and, therefore, the more it will have to be restored.

The main task of medicine has always been to save human life. Actually, for the sake of this noble cause, we entered medical school and this is what we were taught, and we taught it. However, it is equally important to ensure the recovery process after illness and to provide the body with everything it needs. If you think that antibiotics or antiviral drugs(I mean those that actually act on the virus) cure a person from an infection, then you are mistaken. These drugs stop the progressive proliferation of bacteria and viruses. And the cure, i.e. the destruction of what is not viable and the restoration of what was is carried out by cells immune system, endothelial cells and stem cells!

The better the process is provided with everything necessary, the more complete the restoration will occur - primarily the blood supply to the affected part of the organ. This is precisely why the drug LongaDNA was created. It contains L-arginine - a source of NO, vitamins that ensure metabolism inside a dividing cell, and DNA necessary for the full process of cell division.

What is L-arginine and DNA and how do they work:

L-arginine is an amino acid, the main source for the formation of nitric oxide in vascular endothelial cells, nerve cells and macrophages. NO plays main role in the process of relaxation of vascular smooth muscle, which leads to a decrease in blood pressure and prevents the formation of blood clots. Huge value NO has for normal functioning nervous and immune systems.

To date, the following effects of L-arginine have been experimentally and clinically proven:

• One of the most effective stimulants of growth hormone production, it allows you to maintain its concentration at the upper limits of normal, which helps improve mood, makes a person more active, proactive and resilient. Many gerontologists explain the phenomenon of longevity by an increased level of growth hormone in centenarians.
• Increases the speed of recovery of damaged tissues - wounds, tendon sprains, bone fractures.
• Increases muscle mass and reduces body fat mass, effectively helping you lose weight.
• Effectively enhances sperm production and is used to treat infertility in men.
• Plays a significant role in the processes of memorizing new information.
• It is a hepatoprotector – a protector that improves liver function.
• Stimulates the activity of macrophages - cells that protect the body from the aggression of foreign bacteria.

DNA - deoxyribonucleic acid - a source of nucleotides for the synthesis of its own DNA in actively reproducing cells (epithelium gastrointestinal tract, blood cells, vascular endothelial cells):

• Powerfully stimulates cellular regeneration and restoration processes, accelerates wound healing.
• Has a pronounced positive influence on the immune system, enhances phagocytosis and local immunity, thereby dramatically increasing the body’s resistance and immunity to infections.
• Restores and enhances the adaptive capabilities of organs, tissues and the human body as a whole.

Of course, each person has his own unique DNA in his cell, its uniqueness is ensured by the sequence of nucleotides, and if something, just a little - a pair of nucleotides, is missing, or due to a lack of one of the vitamins, some element will be assembled incorrectly - all the work will be in vain! The defective cell will be destroyed! For this purpose, the body has a special supervisory department of the immune system. It is in order for recovery to take place as efficiently as possible, to slow down the aging process, that LongaDNA was created. LongaDNA is food for the endothelium.

The human body consists of many various cells. Some make up organs and tissues, and others make up bones. In the building circulatory system Endothelial cells play a huge role in the human body.

What is endothelium?

The endothelium (or endothelial cells) is active endocrine organ. Compared to the others, it is the largest in the human body and lines blood vessels throughout the body.

According to the classical terminology of histologists, endothelial cells are a layer that includes specialized cells that perform complex tasks. biochemical functions. They line the entire inside and their weight reaches 1.8 kg. Total quantity There are up to one trillion of these cells in the human body.

Immediately after birth, the density of endothelial cells reaches 3500-4000 cells/mm2. In adults, this figure is almost two times lower.

Previously, endothelial cells were considered only a passive barrier between tissues and blood.

Existing forms of endothelium

Specialized forms of endothelial cells have certain structural features. Depending on this they distinguish:

• somatic (closed) endothelial cells;
• fenestrated (perforated, porous, visceral) endothelium;
• sinusoidal (large porous, large window, hepatic) type of endothelium;
• ethmoidal (intercellular slit, sinus) type of endothelial cells;
• high endothelium in postcapillary venules (reticular, stellate type);
• endothelium of the lymphatic bed.

The structure of specialized forms of endothelium

Endotheliocytes of the somatic or closed type are characterized by tight gap junctions and, less commonly, by desmosomes. In the peripheral areas of such endothelium, the thickness of the cells is 0.1-0.8 microns. In their composition one can notice numerous micropinocytotic vesicles (organelles that store useful substances) continuous basement membrane (cells separating connective tissues from the endothelium). This type of endothelial cells is localized in the exocrine glands, central nervous system, heart, spleen, lungs, and large vessels.

Fenestrated endothelium is characterized by thin endotheliocytes, which contain through diaphragmatic pores. The density in micropinocytotic vesicles is very low. A continuous basement membrane is also present. These endothelial cells are most often found in capillaries. Cells of such endothelium line the capillary beds in the kidneys, endocrine glands, mucous membranes of the digestive tract, choroid plexuses of the brain.

The main difference between the sinusoidal type of vascular endothelial cells and the rest is that their intercellular and transcellular channels are very large (up to 3 µm). Characteristic discontinuity of the basement membrane or its complete absence. Such cells are present in the vessels of the brain (they are involved in the transport shaped elements blood), adrenal cortex and liver.

Cribriform endothelial cells are rod-shaped (or spindle-shaped) cells that are surrounded by a basement membrane. They also take an active part in the migration of blood cells throughout the body. Their location is the venous sinuses in the spleen.

The reticular type of endothelium includes stellate cells, which are intertwined with basolateral processes of a cylindrical shape. The cells of this endothelium provide transport of lymphocytes. They are part of the vessels passing through the organs of the immune system.

Endothelial cells, which are found in the lymphatic bed, are the thinnest of all types of endothelium. They contain increased levels of lysosomes and contain larger vesicles. There is no basement membrane at all, or it is discontinuous.

There is also a special endothelium that lines the posterior surface of the cornea human eye. The endothelial cells of the cornea transport fluid and solutes into the cornea and also maintain its dehydrated state.

The role of the endothelium in the human body

Endothelial cells, which line the inside of the walls of blood vessels, have an amazing ability: they increase or decrease their number, as well as their location, in accordance with the requirements of the body. Almost all tissues require blood supply, which in turn depends on endothelial cells. They are responsible for creating a highly adaptable life support system that branches into all areas human body. It is thanks to this ability of the endothelium to expand and restore the network of blood vessels that the healing process and tissue growth occur. Without this, wound healing would not occur.

Thus, endothelial cells lining all vessels (from the heart to the smallest capillaries) ensure the passage of substances (including leukocytes) through tissues into the blood, and also back.

Besides, laboratory tests embryos showed that all large blood vessels and veins) are formed from small vessels, which are built exclusively from endothelial cells and basement membranes.

Endothelial functions

First of all, endothelial cells maintain homeostasis in the blood vessels of the human body. The vital functions of endothelial cells include:

• They act as a barrier between blood vessels and blood, essentially serving as a reservoir for the latter.
• Such a barrier has what protects the blood from harmful substances;
• The endothelium senses and transmits signals carried by the blood.
• It integrates, if necessary, the pathophysiological environment in the vessels.
• Performs the function of a dynamic regulator.
• Controls homeostasis and restores damaged blood vessels.
• Maintains the tone of blood vessels.
• Responsible for the growth and remodeling of blood vessels.
• Detects biochemical changes in the blood.
• Recognizes changes in carbon dioxide and oxygen levels in the blood.
• Ensures blood fluidity by regulating its coagulation components.
• Control blood pressure.
• Forms new blood vessels.

Endothelial dysfunction

As a result of endothelial dysfunction, the following may develop:

• atherosclerosis;
• hypertension;
• coronary insufficiency;
• diabetes and insulin resistance;
• renal failure;
• asthma;
• adhesive disease abdominal cavity.

All these diseases can only be diagnosed by a specialist, so after 40 years you should undergo regular full examination body.

Tatyana Khmara, cardiologist, City Clinical Hospital named after I.V. Davydovsky about a non-invasive method for diagnosing atherosclerosis on early stage and selection of an individual aerobic physical activity program for the recovery period of patients with myocardial infarction.

Today, the FMD test (assessment of endothelial function) is the “gold standard” for non-invasive assessment of endothelial condition.

ENDOTHELIAL DYSFUNCTION

The endothelium is a single layer of cells lining the inner surface of blood vessels. Endothelial cells perform many vascular functions, including vasoconstriction and dilation, to control blood pressure.

All cardiovascular risk factors (hypercholesterolemia, arterial hypertension, impaired glucose tolerance, smoking, age, overweight, sedentary lifestyle life, chronic inflammation and others) lead to dysfunction of endothelial cells.

Endothelial dysfunction is an important precursor and early marker of atherosclerosis, allows for a fairly informative assessment of the selection of treatment for arterial hypertension (if the selection of treatment is adequate, then the vessels respond correctly to therapy), and also often allows timely identification and correction of impotence in the early stages.

Assessment of the state of the endothelial system formed the basis of the FMD test, which allows identifying risk factors for the development of cardiovascular diseases.

HOW IT’S DONEFMD TEST:

The non-invasive FMD method involves a vessel stress test (analogous to a stress test). The test execution sequence consists of next steps: measurement of the initial diameter of the artery, clamping brachial artery for 5-7 minutes and re-measure the artery diameter after removing the clamp.

During compression, the blood volume in the vessel increases and the endothelium begins to produce nitric oxide (NO). When the clamp is removed, blood flow is restored and the vessel expands due to accumulated nitric oxide and sharp increase blood flow speed (300–800% of the original). After a few minutes, the dilation of the vessel reaches its peak. Thus, the main parameter monitored by this technique is the increase in the diameter of the brachial artery (%FMD is usually 5–15%).

Clinical statistics show that people with increased risk development of cardiovascular diseases, the degree of vascular dilatation (%FMD) is lower than in healthy people due to the fact that endothelial function and the production of nitric oxide (NO) are impaired.

WHEN DO YOU NEED TO CONDUCT A VASCULAR STRESS TEST?

Assessing endothelial function is the starting point to understand what is happening to vascular system the body even during the initial diagnosis (for example, the admission of a patient with vague chest pain). Now it is customary to look at the initial state of the endothelial bed (is there a spasm or not) - this allows you to understand what is happening to the body, is there arterial hypertension, is there vasoconstriction, is there any pain associated with coronary disease hearts.

Endothelial dysfunction is reversible. With the correction of risk factors that led to disorders, endothelial function is normalized, which makes it possible to monitor the effectiveness of the therapy used and, with regular measurement of endothelial function, to select an individual aerobic physical activity program.

SELECTION OF AN INDIVIDUAL PROGRAM OF AEROBIC PHYSICAL ACTIVITY

Not every load has a good effect on blood vessels. Too intense exercise can lead to endothelial dysfunction. It is especially important to understand the load limits for patients in recovery period after heart surgery.

For such patients in the City Clinical Hospital named after. I.V. Davydovsky, under the leadership of the Head of the University Clinic of Cardiology, Professor A.V. Shpektra, developed special technique selection of an individual physical activity program. In order to select the optimal physical activity for the patient, we measure %FMD readings at rest, with minimal physical activity and at the maximum load. Thus, both the lower and upper limits of the load are determined, and an individual load program is selected for the patient, the most physiological for each person.

Endothelium is the inner lining of blood vessels that separates the bloodstream from deeper layers vascular wall. This is a continuous monolayer (1 (!) layer) epithelial cells, forming tissue whose mass in humans is 1.5-2.0 kg. The endothelium continuously produces a huge amount of the most important biologically active substances, thus being a giant paracrine organ distributed over the entire area of ​​the human body.

Endothelial functions

The vascular endothelium performs many different functions, including the most important barrier function. It is the first and last frontier where the fate of our vessels is decided. It is he who “kicks” everything that has no place in the wall of the vessel. And vice versa, if it is “broken,” unwanted guests climb into the wall, and a quiet disgrace begins there, which ends in a heart attack.

In the context of this article, it is important for us that all risk factors for the development of vascular diseases, be it smoking, high cholesterol levels or a sedentary lifestyle, “hit” the endothelium, and if it is still “tolerating” - well, keep up the good work - you are lucky with your heredity, and if it fails, you need to change your life.

Also key endothelial function consists of regulating vascular tone, leukocyte adhesion processes and the balance of profibrinolytic and prothrombogenic activity. Decisive role In this case, nitric oxide (NO) formed in the endothelium plays a role. Nitrogen monoxide performs important function in the regulation of coronary blood flow, namely, it expands or narrows the lumen of blood vessels in accordance with the needs of the body.

Increased blood flow, e.g. physical activity, due to the efforts of flowing blood, leads to mechanical irritation of the endothelium. This mechanical stimulation stimulates NO synthesis. If the endothelium is able to produce NO, then it is healthy and its function is not impaired.

Endothelial dysfunction

When the endothelium is damaged, the balance is disturbed in the direction of vasoconstriction. This imbalance between vasodilation and vasoconstriction characterizes a condition called endothelial dysfunction.

Narrowing and constriction of blood vessels is called stenosis. Stenosis occurs due to “plaques” that form on the walls of blood vessels. Such a plaque is a thrombus - a pathological blood clot in the lumen of a blood vessel or in the cavity of the heart. In addition to the usual threat of endothelial dysfunction, the breakdown of these “plaques” leads to such terrible manifestations of atheroskerosis as heart attack, stroke, etc.

Diseases associated with endothelial dysfunction:

1. hypertension,
2. coronary insufficiency,
3. myocardial infarction,
4. diabetes and insulin resistance,
5. renal failure,
6. hereditary and acquired metabolic disorders (dyslipidemia, etc.),
7. thrombosis and thrombophlebitis
8. endocrine age-related disorders,
9. non-respiratory pulmonary pathologies (asthma)

AngioScan technology in relation to endothelial function is based on recording changes in pulse wave parameters that occur after a test with brachial artery occlusion, i.e. on pulse diagnostics. Within 1 minute after 5 minutes of clamping of the artery, we force the endothelium to work and evaluate how it copes with its function of vasodilation (vasodilation).