General characteristics of inflammation

Inflammation - Protective-adaptive reaction of a holistic organism on the action of a pathogenic stimulus, manifested by the development of tissue damage or blood circulation organ and an increase in vascular permeability in combination with dystrophy of tissues and cell proliferation. Inflammation is a typical pathological process aimed at eliminating the pathogenic stimulus and restoring damaged tissues.

Famous Russian scientist I.I. Mechnikov at the end of the XIXVEK first showed that inflammation is inherent not only to man, but also lower animals, even one-cell, although in primitive form. At higher animals and humans, the protective role of inflammation is manifested:

a) in localization and elimination of inflammatory hearth from healthy tissues;

b) fixation in place, in the focus of inflammation of the pathogenic factor and its destruction; c) removal of decay products and restoration of tissue integrity; d) work out in the process of inflammation of immunity.

However, I.I. Mechnikov believed that this protective reaction of the body is relative and imperfect, as inflammation is the basis of many diseases, often ending with the death of the patient. Therefore, it is necessary to know the patterns of developing inflammation in order to actively interfere with its course and eliminate the threat of death from this process.

To refer to the inflammation of any organ or tissue to the root of them latin name Add ending "IT": for example, kidney inflammation - jade, liver - hepatitis, bladder - Cystitis, pleura - pleurisy and. etc. Along with this, the old names of the inflammation of some organs are preserved in medicine: pneumonia is the inflammation of the lungs, Panariums - the inflammation of the nail file of the finger, angina - the inflammation of the oz and some others.

2 causes and conditions of inflammation

The emergence, course and outcome of inflammation in many ways depend on the reactivity of the body, which is determined by age, gender, constitutional features, the state of physiological systems, primarily immune, endocrine and nervous, the presence of concomitant diseases. Important importance in the development and outcome of inflammation has its localization. For example, the brain abscess of the brain is extremely dangerous for life, diphtheria inflammation.

In terms of severity of local and general changes, inflammation is divided into a normal, when the response of the body corresponds to the strength and nature of the stimulus; The hypergic, in which the response of the body for irritation is much more intense than the effect of the stimulus, and the hypergic, when inflammatory changes are defined weakly or not at all expressed. Inflammation may be limited, but may apply to a whole organ or even a system, for example, connective tissue system.

3 stages and inflammation mechanisms

Characteristic of inflammation, distinguishing it from all other pathological processes, is the presence of three consecutive stages of development:

1) alteration,

2) exudations and 3) cell proliferation. These three stages are necessarily present in the zone of any inflammation.

Alteration - Tissue damage - is a starting mechanism for the development of the inflammatory process. It leads to the release of a special class biologically active substances, called inflammation mediators. In general, all changes arising in the focus of inflammation under the influence of these substances are aimed at the development of the second stage of the inflammatory process - exudation. Inflammation mediators change the metabolism, physicochemical properties and fabric functions, rheological properties of blood and function forming elements. Inflammatory mediators include biogenic amines - histamine and serotonin. Histamine is highlighted by Labrocytes in response to tissue damage. It causes pain, the expansion of the microShower and an increase in their permeability, activates phagocytosis, enhances the release of other mediators. Serotonin is released from blood platelets and changes the microcirculation in the focus of inflammation. The lymphocytes are distinguished by mediators, called lymphocins, which are activated by the most important cells of the immune system - T-lymphocytes.

Blood Plasma Polypeptides - Kinin, including Callipers and Bradykin, cause pain, the expansion of the microShospots and an increase in the permeability of their walls, activate phagocytosis.

Inflammatory mediators include some prostaglandins that cause the same effects as kinins, while regulating the intensity of the inflammatory response.

inflammation protective pathogenic

Rearrangement of metabolism in the alteration zone leads to a change in physical chemical properties Tissues and the development of acidosis in them. Acidosis contributes to increasing the permeability of the vessels and membranes of lysosomes, the decay of proteins and dissociation of salts, thereby causing an increase in oncotic and osmotic pressure in damaged tissues. This in turn increases the yield of fluid from the vessels, determining the development of exudation, inflammatory edema and tissue infiltration in the inflammation zone.

Exudation - Output, or sinking, from blood vessels in a liquid type of blood with substances in it, as well as blood cells. Excomuitation occurs very quickly after the alteration and is ensured primarily by the reaction of the microcirculatory bed in the focus of inflammation. The first reaction of microcirculation vessels and regional blood circulation in response to the effect of inflammation mediators, mainly histamine, are spasm arterioles and a decrease in the inflow of arterial blood. As a result, tissue ischemia occurs in the inflammation zone associated with the increase in sympathetic effects. This reaction of vessels is short-lived. Slowing the speed of blood flow and a decrease in the volume of flowing blood leads to a violation of metabolism in tissues and acidosis. Spasm arterioles is replaced by their expansion, increasing blood flow rate, volume of flowing blood and an increase in hydrodynamic pressure, i.e. The appearance of arterial hyperemia. The mechanism of its development is very complicated and is associated with the weakening of sympathetic and increasing parasympathetic influences, as well as with the action of inflammation mediators. Arterial hyperemia helps to increase the metabolism in the focus of inflammation, increases the influx of leukocyte and antibodies to it, contributes to the activation of the lymphatic system, which takes the decomposition of tissue decay. The hyperemia of vessels causes an increase in temperature and redness of the inflammation site.

Arterial hyperemia as inflammation is developing is replaced by venous hyperemia. Blood pressure in venules and postcases increases, the rate of blood flow slows down, the volume of the flowing blood decreases, the venules become convulsions, pecculent blood movements appear in them. In the development of venous hyperemia, the loss of tone of the walls of Volen is matters due to disruption of metabolism and acidisosis of tissues in the focus of inflammation, vesa thrombination, compresses them with educt fluid. Slowing the speed of blood flow in venous hyperemia contributes to the movement of leukocytes from the center of blood flow to its periphery and sticking them to the walls of the vessels. This phenomenon is called edge standing leukocytes, it precedes them to exit vessels and transition to the tissue. Venous hyperemia ends with blood stops, i.e. The emergence of the state, which manifests itself first in Venulah, and later becomes true, capillary. Lymphatic vessels are overwhelmed with lymph, lymphotok slows down, and then stops, since thrombosis of lymphatic vessels occurs. Thus, the focus of inflammation is isolated from intact fabrics. At the same time, blood to it continues to flow, and its outflows and lymphs are dramatically reduced, which prevents the spread of damaging agents, including toxins, by the body.

Excomuitation begins during the period of hyperemia and reaches a maximum in venous hyperemia. The reinforced yield of the liquid part of the blood and substances dissolved in it from vessels into the tissue is due to several factors. The leading importance in the development of the exudation has an increase in the permeability of the walls of the microShosuds under the influence of inflammation mediators, metabolites (lactic acid, ATP decay products), lysosomal enzymes, disorders of the balance of ions to and sa, hypoxia and acidosis. The fluid yield is also due to the increase in the hydrostatic pressure in microsudes, hyperoncia and tissue hyperosmia. Morphologically increased vascular permeability manifests itself in strengthening pinocytosis in the endothelium of vessels, swelling of basal membranes. As the vascular permeability increases from the capillaries to the hearth of inflammation, the shaped elements of blood begin to go out.

The fluid accumulating in the focus of inflammation is called exudate. According to the composition, the exudate is significantly different from the transudate - the accumulation of fluid during edema. In excessive, the protein content is significantly higher (3-5%), and the exudate contains not only albumin, as a transudate, but also proteins with high molecular weight - globuline and fibrinogen. In the exudate, in contrast to the transudate, there are always uniform elements of blood - leukocytes (neutrophils, lymphocytes, monocytes), and often red blood cells, which, accumulating in the focus of inflammation, form inflammatory infiltrate. Exudation, i.e. The current of the vessels from the vessels into the fabric towards the center of the focus of inflammation, prevents the spread of the pathogenic stimulus, the products of the liveliness of the microbes and the decay products of their own tissues, contributes to the inflammation of the leukocytes and other formed elements of blood, antibodies and biologically active substances into the focus. The exudate contains active enzymes, which are released from the dead leukocytes and lysosomes of cells. Their action is directed to the destruction of the microbes, the melting of the remained cells and tissues. In the exudate there are active proteins and polypeptides, stimulating cell proliferation and tissue restoration at the final stage of inflammation. At the same time, the exudate can squeeze the nervous trunks and cause pain, disrupt the function of organs and cause pathological changes to them.

Classification of inflammation on the etiology of inflammation (depending on the type of flood agent):

1. Exogenous factors:

1. Mechanical.

2. Physical (radiation, electrical energy, heat, cold).

3. Chemicals (acids, alkalis).

5. Antigenic (allergic inflammation).

1. Endogenous factors:

1. Fabric decay products - infarction, necrosis, hemorrhage.

2. Thrombosis and embolism.

3. Products of impaired metabolism - toxic or biologically active substances (for example, at Uremia toxic substancesThe resulting in the body is distinguished from the blood with mucous membranes, leather, kidneys and cause inflammatory reactions in these tissues).

4. Deposition of salts or loss of biological compounds in the form of crystals.

5. Nerivo-dystrophic processes.

By participation of microorganisms:

· Infective (septic).

· Non-infectious (aseptic).

Reactivity:

· Hypeirgic.

· Normergic.

· Hypoergic.

With the flow:

· Acute.

· Subacute.

· Chronic.

According to the predominance of the stage:

· Alteractive arises in parenchymal organs (recently denied).

· Exquidative occurs in fiber and vessels (brunt, serous, fibrinous, purulent, rotten, hemorrhagic, catarrhal, mixed).

· Proliferative (productive) occurs in bone tissue.

Stage of inflammation

I. Stage of alteration (damage) happens:

· Primary,

· Secondary.

II. The step of exudation in it includes:

· Vascular reactions,

· Actually exudation,

· Margination and leukocyte emigration,

· Fixed reactions (chemotaxis and phagocytosis).

III. Stage of proliferation (restoration of damaged tissues):

Aukhthonity- This is the property of inflammation when starting, flow through all stages to a logical completion, i.e. The cascade mechanism is activated when the previous stage creates the subsequent.

Local signs of inflammation The Roman Encyclopedist Celsius was described. He called 4 signs of inflammation: redness (Rubor), swelling (Tumor), local fervor (Color), pain (Dolor). The fifth sign called Galen - this violation of function - FUNCTIO LAESA.

1. Redness associated with the development of arterial hyperemia and "arterialization" of venous blood in the focus of inflammation.

2. Heat It is due to an increased influx of warm blood, activation of metabolism, separation of biological oxidation processes.

3. "Tumor" ("swelling") It arises due to the development of exudation and edema, swelling of tissue elements, an increase in the total diameter of the vascular bed in the focus of inflammation.

4. Pain It develops as a result of irritation of nervous endings by various biologically active substances (histamine, serotonin, bradykin, etc.), shearing the active reaction of the medium into the acidic side, the occurrence of dysonia, an increase in osmotic pressure and mechanical stretching or tissue compression.

5. Violation of the function of the inflamed It is associated with the disorder of its neuroendocrine regulation, the development of pain, structural damage.

Fig. 10.1. P. Cull caricature on the description of Dr. A. A. Willoughby classic local signs of inflammation.

General signs Inflammation

1. Changing the number of leukocytes in peripheral blood : leukocytosis (develops with the overwhelming majority of inflammatory processes) or significantly less lakeing (for example, with inflammation of viral origin). Leukocytosis is due to the activation of leukeopoese and the redistribution of leukocytes in the bloodstream. The main reasons for its development include SAR stimulation, the effects of certain bacterial toxins, tissue decay products, as well as a number of inflammation mediators (for example, IL 1, monocytopower induction factor, etc.).

2. Fever It develops under the influence of inflammation coming from the focus of pyrogenic factors, such as lipopolysaccharides, cationic proteins, Il 1, etc.

3. Change of protein "profile" it is expressed in the fact that the so-called "acute phase" proteins "(BOF) inflammation - C-jet protein, ceruloplasmin, gaptoglobin, complement components, etc., accumulate in the blood process in the blood; for chronic flow of inflammation, an increase in the blood of the content of A- and especially G-globulins.

4. Changes in the enzyme composition of blood It is expressed in increasing the activity of transaminases (for example, alaninantransaminases in hepatitis; aspartattransaminases for myocardium), hyaluronidases, thrombocinases, etc.

5. Increase the erythrocyte sedimentation speed (ESO) due to reducing the negative charge of erythrocytes, an increase in blood viscosity, agglomeration of red blood cells, changes in the protein spectrum of blood, temperature rise.

6. Changes in blood hormones It is usually in increasing the concentration of catecholamines, corticosteroids.

7. Activation immune system and allergyizing the body are expressed in the increase in the titer of antibodies, the appearance of sensitized lymphocytes in the blood, the development of local and general allergic reactions.

II. The mechanisms of primary and secondary alteration. Mediators inflammation, their origin and basic effects. The scheme of the formation mechanism in the focus of bradykinin and prostaglandin inflammation.

Primary alteration It is caused by the immediate action of a damaging agent (for example, mechanical injury with a hammer).

For it are characteristic Acidosis of damage, reduction of macroehers, disruption of pumps, accumulation of unsophisticated products, changing the pH, increase the permeability of membrane structures, swelling cells.

Secondary alteration It occurs in the dynamics of the inflammatory process and is due to both the impact of the floodogenic agent and the factors of the primary alteration (mainly circulatory disorders).

For it, it is characteristic Direct effects of lysosomal enzymes (hydrolylase, phospholipase, peptidase, collagenase, etc.), their damaging effect. Mediators, complement system, kininic system have mediated action.

Alteration Manifestations:

1. Violation of bioenergy processes in tissues.

All elements of damaged tissue are responsible for damage: microcirculatory units (arterioles, capillaries, venules), connecting tissue (fibrous structures and cells), obese cells, nervous cells.

Violation of bioenergy in this complex manifests itself in reducing oxygen consumption with cloth, reducing fabric breathing. Damage to mitochondrial cells is an essential prerequisite for these violations.

In the tissues prevailing glikoliz. As a result, the ATP deficiency arises, the energy deficit. The predominance of glycolysis leads to the accumulation of unsophisticated products (lactic acid), arises acidosis.

The development of acidosis in turn leads to violation of the activity of enzyme systems, To disorganization of the metabolic process.

2. Violation of transport systems in damaged tissue.

This is due to damage to membranes, a lack of ATP required for operation potassium-sodium pump.

The universal manifestation of damage to any tissue will always have potassium output from cells, and a delay in sodium cells. With a sodium delay in cells, another heavy or lethal damage is connected - delay in water cells, that is intracellular edema.

Potassium output leads to the deepening of the metabolic disorganization process, stimulates processes education of biologically active substances - mediators.

3. Damage to membranes lysosomes.

Wherein lisosomal enzymes are released. The spectrum of the action of lysosomal enzymes is extremely wide, actually lysosomal enzymes can destroy any organic substrates. Therefore, when they are released, observed female damage to cells.

In addition, lysosomal enzymes, acting on substrates, form new biological active substances, toxic cells acting on cells that enhance the inflammatory response is lizosomal floogogenic substances.

During the alteration, metabolic (hypoxia) or structural changes (mechanical injury) are possible, so two of its pathogenetic mechanism is distinguished:

· Bioenergy damage (ischemia, hypoxia),

· Damage to membranes and transport systems.

Inflamatio (inflamatio) - The standard pathological process developed during the evolution, which is based on the local reaction of a holistic organism on the effect of a damaging (floodogenic) stimulus, manifested at the site of damage to tissue or organ destruction of cells, changes in blood circulation, an increase in vascular permeability in combination with tissue proliferation.

The occurrence and development of inflammation is determined by two factors - local damage to the tissue or organ (alteration) and the reactivity of the body. All factors that can cause local damage and development of inflammation were called floogogenic (Greek. Phlogosis - inflammation).

Etiology inflammation

Floogogenic factors are divided into two main groups: ex- and endogenous. Exogenous factors include mechanical, physical, chemical, biological, immunological conflict that occurs under the action of allergen to a sensitized organism. Endogenous floogogens include deposition of salts, thrombosis, embolism, etc. The division of flogogen on ex- and endogenous conditional, for all the so-called endogenous floogogens arise as a result of exogenous influences.

Depending on the cause of inflammation, the latter is divided into infectious, noncommunicable (aseptic) and allergic.

Signs of inflammation

When analyzing the development of inflammation, morphological, physico-chemical and clinical signs can be distinguished (Table 1).

The first four clinical signs of inflammation were described by Celsios (25 g. BC- 45 G. N.E.). The fifth clinical sign is added by Galen (130-210. N. E.). An important contribution to the study of physicochemical signs of inflammation has made a step; Circulatory disorders, including microcirculation and rheological properties, studied in the works of Y. Konheim and Soviet scientists V. A. Voronina, A. M. Chernukha, D. E. Alperna and their students.

• Alteration and its pathophysiological mechanisms [show] . The alteration phenomena progress as physicochemical aguns form in the focus of inflammation.

  To understand the pathogenesis of inflammation, it is important to know which structures of the organ or tissue are damaged under the action of floogogenic factors. A clear idea of \u200b\u200bthis contributes to the concept of A. M. Chernukh about the functional element of the body. According to this concept, the functional element represents the "spatially oriented structural-functional complex", which includes specialized (for example, hepatic, nervous, muscle) connecting cell elements, blood and lymphatic microcirculatory channel, receptors, afferent and efferent nervous conductors. The functional element is regulated by nervous, endocrine systems and humoral mediators. According to modern concepts, regulation is predominantly humor.

  According to A. M. Chernukha, the activity of the functional element is due to the presence of local and circulating mediators. Local mediators are formed by obese cells and platelets (histamine, serotonin). Special place is occupied by thromboxanes and prostaglandins. The latter are in inactive state in any cell (with the exception of erythrocytes) and are activated when it is damaged. Noraderenalin and acetylcholine formed in adren- and cholinergic nerve endings also belong to local mediators. In the process of vital activity, biologically active substances are also distinguished by polymorphous leukocytes, lymphocytes, macrophages.

  Circulating mediators are represented by kinines, a fibrinolytic system and a complement system.

  Under the action of various flogogen on the functional element of the organ, metabolic and structural disorders of various seventences occur - from small and reversible to extensive, leading cell death. Two pathogenetic mechanisms of acute fatal damage to the cell (A. M. Chernukh, 1979) are distinguished by a violation of the cells and bioenergy cells. It is believed that even a long and significant violation of protein synthesis, nucleic acids without damage to membranes does not lead to cell death.

  Thus, under the action of the phloogenic factor, the permeability of cell membranes and its organelle (mitochondria, lysosomes, and endoplasmic reticulum) increases first. Potassium comes out of the cell, and sodium and water come into the cell and its organelles, which cause their swelling. The swelling of mitochondria is accompanied by the disunity of breathing and oxidative phosphorylation and a decrease in the formation of macroehers, which are especially necessary to maintain the sodium-potassium balance in the cell. Recent changes aggravate the violations of the electrolyte exchange, and the swelling of the cells and its organelle increases. This leads to the discontinuation of the membranes of cells, mitochondria, lysosomes and flow from the latter about 40 hydrolytic enzymes that can cause splitting proteins, fats and carbohydrates. The membranes of organelles are lysed, the nuclei, which leads to the cell fragmentation.

  Most researchers (A. D. ADO, 1973; A. I. Pedkov, 1972; and others) emphasize that under the influence of the inflammatory factor (especially during the formation of arterial hyperemia) in the affected area, oxygen consumption increases, an increase in metabolism and Its subsequent reduction as the circulation disorder is aggravated. With these primary alteractive changes and acute inflammation begins.

• Physico-chemical violations in the focus of inflammation [show]

  Currently, important in the development of inflammation of neutrophils and macrophages is shown. Of these, lysosomal enzymes are exempt not only in the destruction of cells, but also under action on them with 3a and with the 5a components of the complement. At the same time, the cell does not die. Inflammation mediators, immune complexes in the presence of complementary, as well as complement, stimulate the process of lysosomes degranulation. At the same time, CAMF, COLCHICIN, Prostaglandin H oppress the liberation of lysosomal enzymes, is inhibited, thus, further development of inflammation (A. Horst, 1982).

  It is well known that the cell contains 30 times more potassium than in the intercellaneous space, and therefore, in the destruction of cells in the focus of inflammation, the amount of potassium increases and such a physico-chemical sign is formed as hypercalemia. The degree of expression of hypercalemia depends on the intensity of damage to cells. The increase in potassium in the focus of inflammation is 10-20 times (s).

  As a result of an increase in the activity of hydrolytic enzymes, as well as arising later due to the violation of the microcirculation of hypoxia and the predominance of lipolysis, acid-milk, peerograde, amino acids, fatty acids and other pH are accumulated in the focus of inflammation gradually decreased, and n-hyperia is developing. Hydrolysis of proteins, fats and carbohydrates and the increase in the number of molecules in the focus of inflammation provide an increase in osmotic pressure.

  The decomposition of cell elements and the increase in the permeability and exit to the focus of inflammation from the bloodstream of blood proteins, despite the predominance of proteolysis due to the enzymes of lysosomes of cells, cause an increase in oncotic pressure in the focus of inflammation.

  Immediately after the action of floodogenic factors, along with the above-described physicochemical changes, the number of biologically active substances that affect the microcirculatory vessels, the cellular reactions of the inflammation of inflammation are accumulated. All inflammation mediators affect the diameter and permeability of the microcirculatory vessels, on chemotaxis and phagocytosis.

  The first mediators formed during the degranulation of obese cells, basophils and the destruction of the plates are histamine and serotonin. An important biological effect of them is to expand the vessels, an increase in the permeability of capillaries and Volet. Histamine is allocated only at the beginning of inflammation (within an hour), and then disappears.

  In case of damage to the floodogenic factors of the vascular endothelium, the XII plasma coagulation factor (Hageman factor) and a number of proteolytic enzymes (especially plasmin) are activated, and a number of proteolytic enzymes (especially plasmin), which is the formation of the α 2-globulin of the blood of low molecular weight compounds called kinines. Their representatives are Callidin and Bradykin. These are typical inflammation mediators, for, acting on a microvascular course of the functional element, extend the vessels, increase their permeability and participate in the formation of pain. It is shown that in comparison with histamine, Brudikinin increases three times more permeability and is the most powerful pain agent (A. Horst, 1982).

  The activation of blood enzymes at inflammation is chain and even a cascade nature, with each subsequent stage goes faster than the previous one, and the reaction proceeds on an autocatalytic version. In this regard, inhibitors are important. The deficiency of inflammation inhibitors can facilitate the occurrence and weighting of inflammation. For example, an integrator deficiency with 1 complement or C 1 of Esterase leads to excessive activation of the complement system with the release of anaphylotoxin, histamine and other mediators that increase the permeability of blood vessels (A. Horst, 1982).

  It is well known that in any cell (except erythrocytes) is contained in the inactive state of prostaglandins. When cell damage, their activation occurs. The media function with inflammation is performed by the prostaglandins E 1 and E 2. They are formed from arachidon and linoleic acids under the action of prostaglandinscentase enzyme. Prostaglandins Very unstable substances and when passing through the lungs lose 98% of their activity.

  Some prostaglandins inhibit platelet aggregation, separation of serotonin, and also stimulate the formation of the CAMF, which prevents the degranulation of fat cells and the allocation of histamine. All these reactions inhibit the development of inflammation. A natural prostaglandin inhibitor was found in the blood plasma. Under the influence of glucocorticoids, it is activated and, inhibiting the synthesis of prostaglandins, inhibits inflammation (A. Horst).

  Analyzing the formation of inflammatory mediators, the researchers believe that histamine and serotonin are allocated in the earliest stages of the inflammatory response, somewhat later due to the activation of the Kallirin-Kininov system, Callidin and Bradykin are formed. The selection of prostaglandins occurs at the later stages of inflammation.

  Along with the above-described allergic inflammation, a slowly reacting substance of anaphylaxis (MRS-A) and the substance p, causing an increase in vessel permeability, are formed.

  The leukocytes of the focus of inflammation isolated the peptides that called the leukokinins, the main effect of which is to increase the permeability of the vessels and the reduction of systemic arterial pressure.

  An important role of complement is established in the inflammation mechanism. Complement activation occurs in the focus of inflammation of blood antibodies and the C-jet protein, generated during inflammation, as well as substances bacterial origin (lipopolysaccharides, endotoxins), etc. Activation of the complement system represents a enzymatic process, as a result of which such inflammation mediators are formed on cell membranes, as with 2a, with 3a, with 5a, having the properties of kininov, chemotaxis, anaphylactoxine; They exempt lysosomal enzymes and activate phagocytosis, and ultimately activated complement leads to lysis of cells (A. Horst, 1982).

  In addition to the mediators affecting the processes of microcirculation, the permeability of the vessels and the formation of pain, the mediators stimulating chemotaxis and phagocytosis are formed in the focus of inflammation. Recently, the extremely important role of the PM leukocytes in the pathogenesis of inflammation is shown, especially in increasing permeability, necrosis and hemorrhages, which is confirmed by the braking of these effects under leukopenia. The mechanism of pathogenic effects is associated with the formation as a result of their degranulation of cationic proteins or polypeptides, proteases, kininov, MPS-A.

  Cationic proteins cause degranulation of obese cells. With phagocytosis, the leukocytes highlight the permeability factor. Sour proteases or cathpsy lysosomes of PM leukocytes and collagenase hydrolyzed proteins and precipitates antigen - antibody with the formation of active polypeptides.

  As a result of physicochemical changes and especially the formation of inflammation mediators, microcirculation disorders and the rheological properties of blood in the focus of inflammation occur.

• Disorders of microcirculation and hemorology in the focus of inflammation [show]

  A. M. Chernukh (1979), A. I. Stops (1982) allocate three stages of circulatory disorders:

  • 1 stage - short-term spasm and subsequent formation of arterial hyperemia;
  • 2 Stage - venous hyperemia;
  • 3 Stage - blood stas.

  Floogogenic factors cause irritation of the functional element receptors and the reflex reduction of arterioles and prokapillary sphincters, providing short-term ischemia (within 5-10 s to 5 min.). Its development is also due to the action of catecholamines and, probably, serotonin, highlighting platelets from aggregated in microsudes. However, the very rapid histamine, kinines, prostaglandins and other inflammation mediators are expanding arteries and arterioles and ensure the formation of arterial hyperemia. An important role in the development of arterial hyperemia and maintaining it belongs to a change in the sensitivity of α-adrenoreceptors of vessels. According to A. N. Gordienko (1955), Zweifach (1955), the prokapillary sphincters are reduced to the applique of adrenaline 1: 25000. When inflammation due to acidosis, a diistry of a vasoconductive effect of sphincters is reduced. Such a decrease in the reaction to adrenaline and sympathetic effects contributes to the expansion of arterioles and prokapillary sphincters and the formation of arterial hyperemia of inflammatory origin. Inflammatory hyperemia can also develop when irritating the receptors by the axon-reflex type.

  Arterial hyperemia is characterized by an increase in the linear and bulk velocity of blood flow, the number of functioning capillaries. Hydrostatic pressure increases. So, according to Zweifhaha, blood pressure increases in small arteries by 35, the arterioles - by 25, capillaries - at 7, venules - by 9 cm of water column. An increase in blood inflow rich in oxygen contributes to the strengthening of redox processes and heat generation. Therefore, at the stage of arterial hyperemia, an increase in temperature in the inflammation is objectively registered.

  Inflammatory mediators increase the permeability of the vessels and exit to the focus of inflammation of water and proteins of various molecular weight in the following sequence: albumin, globulins, fibrinogen. This process leads to thickening (hemoconcentration), an increase in dynamic viscosity and, consequently, a deterioration in blood flow.

  As a result of the accumulation of the fluid, and later the shaped elements in the tissue are squeezed with lymphatic and blood vesselsWhat makes it difficult for blood outflow. In addition, the vessels develop an aggregation of uniform elements, bonding them and forming sweets. In parallel with this, the rolling system of blood is activated with the formation of thromboms and embolts. All these changes contribute to the further increase in the dynamic viscosity of the blood and the deterioration of the rheological properties of it.

  The reason for the formation of microtrombov and hemorrhage is often direct damage to the wall of the vessels, as well as the effect of mediators (lysosomal enzymes, trypsin, bradykinin, kalline). Hemorrhages are largely due to damage to vessels by proteolytic enzymes, especially PM leukocytes. Erythrocytes leave vessels through inter-endothelial spaces.

  In the venous hyperemia stage, the outflow of blood from the focus of inflammation is disturbed, the consequence of which is the reduction of the linear and volumetric velocity of blood flow, the further increase in the hydrostatic pressure, the development of the peculiar and pendulum-like blood flow, which is associated with an increase in blood flow resistance. Ultimately, a stop (stas) of blood movement occurs. The stas is initially recorded in separate capillaries and venules, in the subsequent, it covers more and more vessels.

  Later, the stasis develops in the arteriols. Depending on the severity of inflammation, the stasis can be short-lived or maintained within hours and days.

• Exudation [show]

  Types and characteristics of exudates Depending on the composition (quality and quantity of proteins, shaped elements), serous, fibrinous, hemorrhagic, purulent exudate is isolated. If each of the listed exudates is infected with putrid microorganisms, it turns into a rotten exudat. Serous exudate [show] Serous exudate is often formed with inflammation of serous cavities of the body (pleural, peritoneal, brain shells, eggs, etc.), in which impairedness and emigration of leukocytes are manifested by nonres. It is also observed in allergic inflammation, insect bites, in the burns of a blister stage, etc. The proportion of such an exudate is greater than 1.018, proteins of the type of albumin and globulins are detected, the pH decreases only to 7.2, the number of leukocytes is about 3000 in 1 μl. Osmotic pressure determined by the point of freezing increases (AC 0.6-1 °). If there are many mucus with inflammation, they talk about catarrhal inflammation. Fibrinous exudat [show] It is formed during diphtheria, scarletin, dysentery, when the permeability of the vessels increases more dramatically and in the exudate accumulates a large-molecular blood protein - fibrinogen. In the focus of inflammation from may be coated with the formation of a fibrin film. Hemorrhagic exudat [show] It occurs with a sharp damage to the vascular wall, which leads to the exit of the erythrocyte vessels and the formation of hemorrhages. Hemorrhagic exudat is observed with a chum, the Siberian ulcers, the phenomenon of Schwartzman, Artus. Purulent inflammation [show] It occurs in extensive inflammatory processes, especially caused by strepto, staphylococci and other biological floogogens. Increased chemotactic substances contribute to the output of a large number of leukocytes and leukocyte infiltration. As a result of a sharp decline in pH, many polymorphous leukocytes are dying, and at a pH 6.7 all types of leukocytes die. A large amount of hydrolytic enzymes is distinguished from the lysos, which cause lysis leukocytes, cleavage of proteins, fats and carbohydrates. The purulent melting and the formation of pus. Glome is predominantly neutrophilic leukocytes at various stages of destruction. They are the so-called purulent tales. Purulent inflammation is characteristic of a furuncle, carbuncule, phlegmon, abscess, empynes. Purulent inflammation can be subject to mucous membranes. In the gnome often contains colonies of microorganisms, fungi.

  Excidation mechanisms

  Extraction is the yield of the liquid part of the blood into the focus of inflammation. There are two phases of increasing permeability (3. Movet, 1975).

  1. Instantly growing permeability of vessels caused by the action of vasoactive mediators.
  2. Late (slow and long) vascular permeability (within hours) associated with the predominant effect of PM leukocytes.

  Their granules contain a number of biologically active substances that are exempt in degranulation and phagocytosis. The process of accumulation of PM leukocytes and degranulation of their lengthy. That is why they provide the slow motion phase of increased vascular permeability. Late phase is suppressed against the background of experimentally reproduced leukopenia.

  Estation in the focus of inflammation is due to direct damage to the vessels of the microcirculatory channel and the effects of inflammation mediators.

  Exdation is carried out in three ways; Through the inter-endothelial slots, the size of which increases by reducing the microfirillace of endothelial cells, through the body of endothelial cells by specialized channels, as well as micropineopitosis in the form of active clearance of the smallest drops through the body of the cell. To emphasize the process of conducting fluid, the term cytopemsis is proposed (cellular suction or conducting, transmission using cells). Until now, the yield of water and solutions through the basal diaphragm of capillaries remains not completely clear.

  According to the mechanism of development, the seduction is due primarily to the effects of inflammation mediators (histamine, serotonin, kinines, prostaglandins, etc.), as well as PM leukocytes. An increase in hydrostatic pressure is important. For example, for stagnation Permeability increases by only 2-4%, but in conditions of inflammation, the combination with an increase in permeability caused by mediators is a significant contribution factor.

  At the later stages of inflammation, the exdtion is due to an increase in osmotic and oncotic pressure in tissues.

  In case of exisudation, water, salts, fine molecules (mol. Weight 1000) are freely through the pores of endothelial cells. Macromolecules are transported in the form of pinocytous bubbles of endothelium or through inter-endothelial gaps.

  Important in the development of inflammatory edema belongs to the lymphatic microcirculatory bed. There are non-permanent communication with incisionable fabric channels Inconsint with terminal lymphatic capillaries. When the channels are filled with intercounted liquid, they seem to be emptied into the inter-indocent holes, fall and separated from the capillaries, and the inter-endothelial slots are closed. They consider (A. I. Strakov, 1983) that, due to this, filtering, reabsorption of tissue fluid, proteins, salts and homeostasis is maintained. When inflammation, endotheliums of primary lymphatic capillaries are damaged. This leads to the dishee of the outcast tissue channels from the inter-endothelial gaps, the lymph goes into the cloth. So in early period Forms and remains pronounced to the end of inflammation lymphatic swelling.

  Starting from the stage of arterial hyperemia and especially in the stage of venous hyperemia and the leukocyte, the vascular channel leaves. The exit of leukocytes from the vessels in the focus of inflammation is called the emigration of leukocytes.

• Emigration of leukocyte [show]

  Ways and mechanisms of leukocyte emigration . Even I. I. Mesnikov, studying the sequence of leukocyte, noted that polymorphonuclear leukocytes appear first in the focus of inflammation, then mono- and lymphocytes. The leukocyte exit is preceded by the entry movement and the onset standing of leukocytes, observed especially clearly in the stage of venous hyperemia. This phenomenon is explained by a decrease in the negative charge of leukocytes, as well as intense microsinking, as a result of which microfibrillers inhibit the movement of leukocytes and contribute to their clutch standing.

  According to modern data, the leukocytes are emigrated by two ways: polymorphic leukocytes exit through inter-endelial slots, and mononuclearlaras (mono- and lymphocytes) through the body of endothelial cells. The last process is more durable and to some extent explains why mononuclears later appear in the inflamed area. The yield of the PM leukocyte lasts 2-8 minutes. The process of emigration of PM leukocytes reaches the greatest intensity after 6 hours (G. 3. Movet, 1975; E. R. Clark, E. L. Clark, 1935). Mononuclearas begin to emigrate after 6 hours with a maximum of their output 24 hours after damage. The ratio between polymorphoid leukocytes and mononuclearnes in the inflammation dynamics is shown in Figure 1;

  

  A pH of the focus of inflammation also has a certain effect on the sequence of emigration. According to Menkina, with a pH of 7.4-7.2, polymorphoid leukocytes accumulate, at a pH of 7.0-6.8, predominantly mono- and lymphocytes. With a pH 6.7 in the focus of inflammation, all leukocytes are dying with the formation of pus.

  It is important in the emigration of leukocytes belongs to Chemotaxis, i.e. the presence of chemical sensitivity, which ensures the directional movement of leukocyte to a foreign object or chemical substance (positive chemotaxis) or, on the contrary, the removal from them (negative hemotaxis) (I. I. Mesnokov). The formation of chemotactic factors occurs when the antigen is interacted by the antibody to form the thermolar components of the complement with 3a and C 5a. The use of complement inhibitors prevents vessel damage and leukocyte output. Chemotaxis is stimulated by streptokinase. At the same time, as a result of splitting with 3a and C 5a, chemotactic factors are formed by a molecular weight of 6000 and 8500, and when activated from 5, C 6, C 7 - chemotactic substances with even greater molecular weight.

  Chemotaxines also appear in infectious inflammation due to endotoxins, with mechanical damage to the tissue. In these cases, the accumulation of a chemotactic factor with molecular weight of about 14,000 is noted. Chemotaxins are also formed by lymphocytes and as a result of protein decay, especially γ-globulins. According to A. M. Chernukha (1979), Chemotaxis can be stimulated by the products of tissue metabolism, bacteria, viruses, as well as a number of blood plasma factors (especially the enzymes of the kallicrein and plasminogen activator).

  A certain value in the emigration of leukocytes belongs to changing their charge. According to A. D. ADO (1961), in the blood of the leukocytes have a charge of 14.6 Milvololt, and in the focus of inflammation only 7.2 Milvololt. Penetrated through endothelium leukocytes for some time delayed in front of the basal membrane and under the action, probably enzymes, especially collagenase, split areas of the basal membrane and fall into the focus of inflammation, accumulating there (A. I. Strankov, 1982).

  Thus, as a result of the outlet of water, proteins and uniform elements, inflammatory exudat is formed. Excudate is a consequence of only the inflammatory process.

• Phagocytosis in the focus of inflammation [show]

  An important manifestation of inflammation is phagocytosis described by I. I. Mesnikov in 1882. Phagocytosis (from Greek. Phagein - absorb) lies in the absorption and digestion of bacteria, products of damage and decay of cells. Phagocytic activity is manifested by microphages (neutrophilic leukocytes) and macrophages.

  Four stage of phagocytosis are distinguished:

  • The 1st stage is the approach of phagocyte to the foreign object. The basis of this movement is the phenomena of chemotaxis leukocytes. Immuno-1 adherence contributes to the directional movement of leukocytes, i.e. the formation of the antigen complex - antibody. As antigen in the focus of inflammation, bacteria and viruses are performed with simultaneous activation of the complomation with 3a and C5a and the formation of chemotaxins. As already mentioned, chemotactic factors arise in damage by other floodogenic factors.
  • The 2nd stage is the adhesion of phagocyte to the object. He is preceded by OPSonization. i.e. with immunoglobulin coating M and G, and fragments of Complement C3, C5, C6, C7 bacteria and damaged cell particles, making them acquire the ability to adhere to phagocyt. The adhesion process is accompanied by an increase in the metabolic activity of leukocytes, its aerobic and anaerobic glycolysis and an increase in oxygen absorption 2-3 times.
  • The 3rd stage is the absorption of the phagocytable object by invagining the phagocyte and the formation of vacuole - the phagemsomas. The formation of the FAGOSOMIs is preceded by an increase in metabolism with an activation of Nadn-dependent oxidase, which ensures the synthesis of hydrogen peroxide. As a result of the degranulation of leukocytes, lysosomal enzymes and bactericidal proteins are distinguished. The hydrogen peroxide decomposes under the influence of peroxidases to form an active oxygen molecule, which interacts with the components of the cell membrane, destroying it by peroxidation.
  • The 4th stage is intracellular splitting and digestion of phagacy-trained microbes and remnants of damaged cells (Table 2).

  Table 2. Enzymes contained in the granules of "professional phagocytes" (according to A. M. Chernukhu, 1979)
  The name of the enzyme	PM leukocyte	Mononuclear Phagocyte
  Protease:
  katepes	+	+
  histonose	+
  leukoprotea	+
  collagenase	+	+
  elastasa	+	+
  Carboradases:
  lizozyme	+	+
  β-glucuronidase	+	+
  haluronidase		+
  Lipases:
  acute Lipasa	+	+
  phospholipase	+	+
  RNA-Aza	+	+
  DNA Aza	+	+
  aclest phospotal	+	+
  alkaline phospotal	+	+
  Neferments:
  cationic proteins	+	-
  leiccitarian Pirogen	+	-
  mukopolisaccharides	+	-

  Only the dead microbes and cells are exposed to digestion. Phagocytosis is carried out with the help of hydrolytic enzymes (proteases, carbohydases, lipases, etc.). Along with the digestion of foreign objects and damaged cells under the influence of hydrolytic enzymes that are distinguished in the Fagosoma, the phagocytes themselves are dying, being the source of the formation of pus, and the products of destruction stimulate the processes of proliferation in the focus of inflammation.

  Depending on the localization of the focus of inflammation, the participation of various macrophages. In the connecting tissue, these are histiocytes, in the liver - krafe cells, in the lungs - alveolar phagocytes, in lymph nodes and spleen - free and partially fixed macrophages, serous cavities - Peritoneal and pleural macrophages, in bone tissue - osteoclasts, nervous system - microglyal cells. All listed macrophages are derivatives of the stem blood-forming cell of the monoblastic series and have high phagocytic activity. The macrophages of the inflammatory exudate are accumulated by the emigration of monocytes (A. I. Strakov, 1982). Macrophages carry out phagocytosis similarly to neutrophilas and have the ability to secreted into the focus of inflammation of lysosomal enzymes, plasmin, collagenase, elastasia, lysozyme, complement proteins, interferon, etc. It is shown that the monocytes are in their membrane receptors for IgG and complement, which after phagocytosis disappear and again. Appear in a few hours. The monocyte membrane is also able to bind with cytophilic antibodies (IgE). Macrofami belongs to the most important role in cleansing the focus of inflammation from the dead cells and the destruction of the substances of antigenic nature, as well as in the formation of an immune response.

  The exceptional value of phagocytosis in the pathogenesis of inflammation is particularly clearly detected in its violation, because even the coil microorganisms can cause sepsis. Phagocytosis in this case is the character of unfinished, and microbes, entering leukocytes from the focus of inflammation into various organs, provide the phenomenon of sepsis. In hereditary enzymopathy, due to the recessive genome adhered to the X-chromosome, there was a decrease in the activity of nuclear-dependent oxidase and, as a consequence, the deficiency of the formation of hydrogen peroxide (H 2 O 2) and, ultimately, the active oxygen molecule cannot be formed. Membrane bacterial cell Not damaged. Phagocytosis remains unfinished. This leads to chronic inflammation, especially in the lungs, to the destruction of the fabric and death of the body. Phagocytosis disorders were found in cirrhosis of the liver, glomerulonephritis, which is due to the activation of chemotaxis inhibitors in sufficient emigration of leukocytes, they may cause chronic inflammation or even sepsis. Phagocytosis braking is detected in diabetes mellitus, hypercorticism, thyroid pathology.

• Proliferation in the focus of inflammation [show]

  As a result of emigration, leukocytes accumulate in the focus of inflammation, and this phenomenon received the name of inflammatory infiltrate. Leukocytes perform phagocytic function for several hours, and then dying. Initially, neutrophils die, and later macrophages, but the last to death provide cleansing due to the phagocytosis of the focus of inflammation from microorganisms. With cell death, substances can be stimulated to stimulate cell proliferation. They got the name of Trefons. Under the influence of trifons, fibroblasts, endothelial cells, which form the so-called granulation tissue, are beginning to form a so-called granulation tissue, which is the outcome of the connecting and intestine scar. Moreover, many specialized cells (liver, muscle, nervous) are usually not regenerated, and therefore one of the most frequent outcomes of inflammation may be the substitution of the cells damaged with ripe fibrous connective tissue, and in the nervous system by glial cells. Thus, one of the outcomes of inflammation is the formation of a scar.

  If alternative changes for the action of the phloogenic factor are minor, the inflammatory process may end with the full restoration of the morphology and the function of the organ. If inflammation (for example, lungs, liver, brain, kidneys) is accompanied by violations in the body incompatible with life, it ends with his death.

The total pathogenesis of inflammation is presented in Scheme 18.

The origin of clinical signs of inflammation

• Redness (Rubor) - due to the development of arterial hyperemia, increasing blood flow with increased content oxygen, increasing the number of functioning capillaries.
• Plowness (TUMOR) is explained by arterial and venous) hyperemia, exdtion, leukocyte emigration.
• Fire (Calor) - due to the enhancement of metabolism on early stages inflammation, blood flow with a higher temperature (especially with inflammation of the skin and mucous membranes, the enhancement of heat transfer due to hyperemia).
• Pain (Dolor) is caused by irritation of receptors in the focus of inflammatory inflammatory inflammatory (especially kinines and prostaglandins, a change in pH, osmotic pressure, dili, mechanical irritation of receptors as a result of swelling in the focus of inflammation).
• Functio Laesa. When inflammation, cell damage, metabolic disorder, blood circulation, accumulation of inflammation mediators, changes of electrolyte balance, pH, osmotic and oncotic pressure, processes of proliferation are noted. Under these conditions, the function of the components of the functional element, and, consequently, the organ is impossible.

Experimental inflammatory models

Under the experimental conditions, inflammation can be reproduced under the action of any floodogenic factor.

• Infectious inflammation is modeled by subcutaneous, intramuscular, intra-limited introduction of living or autoclaved intestinal, abdominal chopsticks, streptot, staphylococcus and other microorganisms.
• Aseptic inflammation is caused by the introduction of subcutaneously or intramuscularly of turpentine, gasoline, kerosene and other substances.
• Allergic (immune) inflammation is modeled more difficult. Animal (rabbit, dog, guinea pig) It is pre-sensitized by three-time administration (subcutaneously, intravenously, subcutaneously) with an interval of 24 hours of serum (bovine, horsepower) or twice the subcutaneous introduction of BCG. After 2-3 weeks, the maximum sensitization severity occurs due to immunological shifts. Introduction At this time allergen is subcutaneously, intramuscularly or in any organ contributes to the immunological conflict, which is the cause of allergic inflammation.

  To simulate auto allergic inflammatory processes, the extracts of organs (heart, kidney, brain) are injected with an experimental animal (heart, kidney, brain) in a pure form or with filler. This is exactly the modeling of lesions of the heart, brain, kidneys and other organs.

Reactivity and inflammation

The occurrence and development of inflammation, as well as its outcome is determined by the reactivity of the body. In particular, the functional state of the nervous system has important in the formation of inflammation. In a state of sleep, winter hibernation of animal inflammation, although developing, but less pronounced, because vascular reactions, exduction and emigration of leukocytes are weakened. The possibility of playing inflammation in people with redness and swelling phenomena by hypnotic suggestion is described. The role of the sympathetic and parasympathetic departments of the vegetative nervous system in the pathogenesis of inflammation is shown in the works of D. E. Alperna. Desimparateization was called in dogs to the right in the lumbar region. Ten days later, inflammation on the inner side of both hips was simulated by applying to the skin for three minutes of flat-bottomed tubes of the same diameter with boiling water. On the desimpact side, inflammation was expressed more, but less was necrotic changes, and the healing process was occurring earlier (for 4-5 days) compared to the control area. A similar effect was observed with the introduction of acetylcholine. When irritating the sympathetic nerves, the inflammation flows sluggishly and more than a long time. The braking of inflammation is also established with the introduction of adrenaline and sympathomimetics - tetra-hydro-β-naphthyl amine.

The endocrine system, being an important mechanism of reactivity, also significantly affects inflammation. In the glomerular zone of adrenal cortexes, mineralocorticoid aldosterone is formed, which, with excessive secretion, changes the water-electrolyte balance of the body, enhances and accelerates the flow of inflammation, which manifests itself in increasing the permeability of vessels, exduction, emigration and phagocytosis, cell proliferation. Excess form of thyroxine and triiodothyronine in thyroid gland And the associated strengthening of redox reactions accelerates inflammation. Thus, aldosterone and thyroid hormones during their excessive formation have a pro-inflammatory effect. On the contrary, excessive administration from the outside or hypersection in the body of glucocorticoids has an anti-inflammatory effect, for these substances reduce the permeability of membranes, the exdtion and emigration of leukocytes, phagocytosis, the formation of inflammatory mediators, depress immunity as a result of braking mitoses, including lymphoid cells, and lead to involution Timic-lymphatic system. Insulin itself does not have a significant influence on inflammation, but in conditions of its deficiency (for example, with diabetes mellitus), counter-culberry hormones are activated, especially glucocorticoids. At the same time, immunity weakened and fungal and often arise infectious diseasesEspecially furunculosis, which often ends with a fatal outcome. Glucocorticoids also slow down the proliferative processes in the focus of inflammation.

Insufficient efficiency immunological mechanisms In children and in high age, the inhibition of immunity immunosuppressants, the starvation is the cause of inflammation, as a result of which infectious processes proceed atiypically or, as in childhood, end with the formation of an ancient form of an infectious process - sepsis. Therefore, the formation of any purulent focus on the skin of the child requires immediate treatment (N. T. Grisova, E. D. Chernikov, 1975).

Common reactions when inflammation

Depending on the intensity and localization, inflammation may be accompanied by common reactions In the form of violations of nervous and endocrine systems, including sympathy-adrenal and hypothalamic-pituitary-adrenal and hypothalamic-pituitary-adrenal system, the development of fever, leukocytosis, changes in the metabolism in the body. Usually, with inflammation as a result of the participation of macrophages in resorption of alien antigens, immunity is stimulated. Ultimately, a violation of the functions of various organs and systems of the body is possible.

Biological value of inflammation

From a osciliation point of view, the inflammatory response was developed during evolution and therefore is a protective-adaptive one. Already the fact that a local infectious process was formed to change the ancient form of infectious process in the form of inflammation, testifies to the protective role of the focus of inflammation. Fixation in the focus of inflammation of biological pathogens occurs due to the disorders of blood and lymphorage as a result of phagocytosis, immunological reactions, as well as the bactericidal action of the excess and enzymes for microorganisms, which die and resorvate. In addition, it is necessary to take into account the sharply increased permeability of the vessels, as a result of which microorganisms and alien substances can be intensively stand out in the focus of inflammation and exposed to destroy and resorption. Finally, the protective value of the focus of inflammation is also manifested in the fact that due to the inflammatory and regeneration in the focus, the functional element is restored, at least even by the scar. At the same time, the altheration in the focus of inflammation leads to a violation of specialized cellular elements, which are usually not regenerated and replaced with a fibrous tissue with impaired fabric functions or organ. Therefore, inflammation is often used to treat anti-inflammatory funds.

General principles of pathogenetic therapy of inflammation

Inflammation is a chain of causal relations, where the previous link affects the subsequent and ultimately for proliferation, the consequence of the formation of scar (fibrous) changes. Therefore, the anti-inflammatory agents used for treatment can influence one or more units of pathogenesis of inflammation (stabilization of diaphragm lysosomes, braking of the formation of mediators of inflammation, permeability of vessels, emigration, phagocytosis, and even proliferation), inhibiting inflammation in general.

Depending on the nature of inflammation, specific and nonspecific therapy is used. The first is aimed at the destruction of the biological pathogen (antibiotics, healing serum, anti-tuberculosis agents, etc.), which possess both bactericidal effects, and, by being an integral part of the metabolic of the substances of the microorganism, violate its livelihoods, facilitating destruction and phagocytosis. Therefore, the destruction of microorganisms or the prevention of the action of allergen is one of the important tasks in the prevention and treatment of infectious and allergic inflammation.

TO non-specific impacts The influence of the modified temperature, irritating substances on inflammation. Heat (dry and wet, hot paraffin, ultrasound), as well as irritating means (mustard pieces, banks, lubrication with turpentine, iodine) improve blood and lymph formation, increase hyperemia, exombtion, leukocyte emigration, phagocytosis, which ensures enhancement and acceleration of inflammation. The cold, on the contrary, inhibits the above-mentioned links of the pathogenesis of inflammation and thus oppress its intensity.

The anti-inflammatory effect of antihistamine drugs is due to braking mobilization or blockade of histamine receptors of metabolic vessels, as a result of which the extension of blood vessels and permeability is inhibited, especially Vull.

According to A. Polycar (1969), A. M. Chernuha (1979), aspirin, amidopin, phenylbutazone stabilize the membranes by lysosomes and inhibit the formation of mediators - kinines, prostaglandins serotonin, histamine, permeability factor. Indomethacin and Bruphen, which act 10-30 times more efficiently for phenylbutazone and aspirin have a stronger anti-inflammatory effect. In addition, aspirin, phenylbutazone, indomethacin prevent protein denaturation and have anti-frequency activity. A number of anti-inflammatory substances like flavonoids (Rutin, Vehoruturt, etc.) reduce vessel permeability, improve blood rheology and venous blood circulation.

For the treatment of inflammation, especially allergic, glucocorticoids are widely used, for they provide the stabilization of diaphragm lysosomes, the decrease in permeability, the exisudation and emigration of leukocytes, phagocytosis, oppress the immunity and proliferation of cells in the focus of inflammation, this in general is inhibits inflammation and at the same time causes sluggish Healing wounds. Given the above effects, glucocorticoids are most widely used in allergic inflammation. Immunosuppressants (alkylating compounds, cyclophosphamide, 6-mercaptopurine, etc.), braking mitosis and angry immunity, suppress inflammation, especially allergic.

Widespread use in the treatment of inflammation found proteolytic enzymes - pepsin, trypsin, chemotripcin. They most effectively purify the wound surface and thus accelerate wound healing and their granulation. On the contrary, antiproteza drugs are ε-aminocaproic acid, tracilol, hydrogen and others have an anti-inflammatory effect.

Thus, the basis of pathogenetic therapy of inflammation is suppressing or stimulation of one or more stiments of pathogenesis of inflammation.

A source: Ovsyannikov V.G. Pathological physiology, typical pathological processes. Tutorial. Ed. Rostov University, 1987. - 192 p.

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Ministry of Health of Ukraine

National Pharmaceutical University

Department of Pharmacology

Abstract on the topic:

"Mediator inflammation - Bradykin"

Performed:

Student 3kursa

Both Ekaterina

Kharkov-2010.

Introduction

Pain for patients is one of the most important clinical signs of any pathological process and one of the most negative manifestations of the disease. At the same time, timely and correct assessment of pain syndrome helps the doctor to make an idea of \u200b\u200bthe nature of the disease.

The concept of pain includes, firstly, a peculiar feeling of pain and, secondly, the response to this feeling characterized by a certain emotional color, reflex changes in functions internal organs, motor unconditional reflexes and volitional efforts aimed at eliminating pain.

The pain reaction is extremely individual, as it depends on the influence of factors, of which localization, the degree of damage to the tissues, the constitutional features of the nervous system, the upbringing, the emotional state of the patient at the time of applying pain irritation are.

Of all kinds of sensitivity, the pain occupies a special place. While other sensitivity as an adequate stimulus has a certain physical factor (thermal, tactile, electric, etc.), the pain signals such conditions of organs that require special complex adaptive reactions. For pain there is no single universal stimulus. As a general expression in human consciousness, the pain is caused by a variety of factors in various organs.

Kinina

Currently, Kininam gives extremely important in the origin of the painful sensation. The teaching on pain mediators has enriched not only by new experimental facts, but also extremely important theoretical provisions.

Our ideas about the terrible action of histamine demanded a revision. In any case, he was not the only (and not even the main thing) a pain mediator.

Fig. 21. The intensity of pain when applying various biologically active substances to the bottom of the Cantaridine Bubble . 1 - acetylcholine - 10 -4; 2 - acetylcholine - 5 10 -5; 3 - fresh plasma; 4 - plasma, standing 4 minutes. in a glass tube; 5 - acetylcholine - 10 -3; 6-- serotonin - 10 -6; 7 - Bradyikinina - 10 -6

Kinina - complex protein-like connections - polypeptides, sometimes called kinin hormones, or local hormones. Kinines, directly related to the problem of pain, are primarily bradykin, Kallidin, as well as I. enterotoxin Famous called substance R.. Kinines have an extremely strong effect on the animal organism. They expand the vessels, increase the rate of blood flow, reduce blood pressure and, especially important, cause pain in contact with chemologyceptors.

These substances are found in the poisons of some snakes, bees, OS, scorpions. They are formed in plasma in the process of blood coagulation, are contained in the skin, glands, inflammatory exudates, etc. The origin of kininov is quite complex. The blood contains the predecessors of Kininov - KININOGEN. Under the influence of specific enzymes - Kallikreins - KININOGEN turn into kinines. In normal physiological conditions, Kinina is rapidly destroyed by special enzymes - kininoses.

Bradikinin is the greatest interest in the problem of pain. This is nonpepeptide, i.e. The ninth peptide, which includes five amino acids: serine, glycine, phenylalanine, proline and arginine. Bradykinin content in blood plasma is negligible. It is not entirely clear which goal is Bradykinin in the body, but the fact that it is constantly contained in the urine, speaks of his physiological role. The value of Bradyikinina in the occurrence of pain does not cause a doubt currently.

Callidin

Another terrible KININO - Callidine - consists of ten amino acids. This is a decapeptide. In the urine, Callidine is absent, as it turns into a bradykin. Bradykinin has a strong influence on vascular system. In this regard, it is many times more active than histamine. Like histamine, Bradykinins sharply increases vessel permeability. If it is introduced into the thickness of the skin, a pronounced swelling occurs almost immediately. Among all the well-known vasculating substances Bradykinin is the most powerful. But he actually acts on pain receptors. Enough to enter B. sleepy artery. 0.5 μg bradykinina to cause severe pain first in the field of thyroid gland, then in jaws, temples and outdoor ear.

As a rule, a person is experiencing particularly sharp pain if Brudikinin in the artery is introduced. Introduction to Vienna is not so efficient, pain in these cases is not so strong and lasts long. The painful pains arise in the formation of Bradykinin and Callinin in inflammatory foci. Apparently, the pain that we experience in various types of inflammation is related to the formation of kinines.

The solution of chemically pure bradykinin causes the strongest painful sensation when applied to the base of the cantaridine bubble in the dilution of 10 -7 - 10 -6 g / ml.

If you enter Brudikinin a dog in the artery, it begins to fight in the straps, seeks to escape from the hand of the experimenter, bite it, she screams, wriggles, moaning. Blood pressure rises, breathing is expensive. The American scientist Lim at the International Congress of Physiologists in Tokyo in 1965 demonstrated a film in which Bradikinina's action was shown when it was introduced into the artery of the dog. All those present in the demonstration hall had the opportunity to observe which painful pain is experiencing an animal.

The intradermal introduction of Bradikinin is also the cause of burning pain, which occurs after 2--3 seconds. After injection. We have already said that blood plasma, standing 5 minutes. In a glass tube, when applied to the bottom of the cantaridine bubble, causes severe pain. This pain is caused by bradykinin, formed when plasma contact with glass. But the plasma, which was in the same test tube of about 1.5 hours, no pain causes. Kinina collapsed under the influence of enzymes - kininas.

Education Kininov

Education and disintegration of kinines in human organism Closely related to blood coagulation system. KININOGEN, predecessors of kininov - proteins formed in the liver - can be isolated from the blood and tissues of human, as well as all types of animals, with the exception of birds. In the blood plasma, they are contained in the alpha-2-globulin fraction. Under the influence of the enzyme, Kallikreine KININOGEN turn into kinines. However, the active kallicrein in the blood is absent. In plasma, it is in inactive form (kallicreogen), which turns into kallicrein under the influence of one of the numerous factors (Factors of Hageman) participating in complex process Blood coagulation. In animals that have a Factor Hageman (for example, a dog), kinin, when contacting plasma with glass, are not formed.

Thus, Kinina (Bradykin, Callidin and some other polypeptides) - Pain Promoting Substances (PPS - PAIN Promoting Substances) - begin their lives in the body at that moment when the first call sounds, hearing the mobilization of the blood coagulation system In vessels or tissues, dried, impact, injury, burn, etc. But it turns out that their education is connected not only with blood coagulation, but also with the dissolution of the fibrin bunches formed. The enzyme dissolving fibrin is plasmin - also takes part in the formation of kinines, activating the kallicinogen and turning it into kallicrein.

Almost immediately, when the intake of tissues is broken and the blood comes in contact with a plot, where the tissue catastrophe has just occurred - in some cases limited, in other extensive, the chain reaction of mobilization of kinino-forming factors begins. It proceeds slowly, graveyard. The maximum number of kinines is detected only after 15-- 30 minutes. And gradually, as the chemistry of tissue changes, the painful sensation begins to increase. It takes some time to achieve the top.

Lyuche showed that the inflammation accompanied by the pain passes in its development two stages. The first accumulate histamine, serotonin, partly acetylcholine, in the second - kinine. At the same time, histamine contributes to activating the kinin system. Histamic pain How would go to kinin. The relay moves from one algorod substance to another. Pain generates pain.

Of course, the body is not defenseless before the Terrible Natius of Kininov. There are many means of protection, overwhelming, neutralizing, compensating for their action. So, from the liver and easy gland The bull was able to allocate the drug, inactivating Kallikrein and, consequently, preventing the transformation of kininogen to kinines. This drug called tracilol, often significantly softens heavy painfulness, improves the condition of the patients and even reduces the number of deaths from the shock caused by unbearable pain. Some authors argue that various antimorphs are phenylbutazone, 2: 6-dihydrobenzoic acid, aspirin, salicylic sodium - prevent the transformation of kininogen to kinines.

But what is the value of kininov in the occurrence of pain syndrome in some diseases, the reasons for which sometimes cannot solve the most experienced doctors?

Bradikinin value in the body

Let's start with the fact that Bradykinin causes pain in the dilution of 10 -7 g / ml. This corresponds to 100 nanograms, i.e. 1/10 000 000 G. With some inflammatory processes in the joints, their fluid fills in 1 ml on average 50 nanograms of bradykinin. As the number of bradykinin or the kalline in the articular liquid increases, the pain in rheumatic lesions is becoming more and more intense. The more kinines, the most painful pain. And this applies not only to the joints, but, essentially, to all organs and tissues of our body.

It would seem that it is enough to neutralize the kinines - in pain will stop. But, alas, the climbing agents in the body are not exhausted not to histamine, nor serotonin, nor kinines. The nature is inventive. For her, pain is a means of self-defense, a line of defense, a danger signal, in many cases a warning of fatal outcome. And nature is not limited to two or three pain signaling mechanisms. Defense should be reliable. Let it be better than the lack of physiological protection measures.

Of great importance for the occurrence of pain, a special substance contained in the intestines and the brain, and the substance called P. In the intestine and the brain, and the Polypeptides also belong to the polypeptides and consists of several amino acids: lysine, asparty and glutamine acids, and consists of several amino acids: lysine, aspartic and glutamine acids, Alanine, Leucine and Isaoleycin. It is close to bradykinin, but for a number of chemical properties is different from him.

Substance P can be selected from the gastrointestinal tract. But all the departments of the central nervous system and the rear (sensitive) spinal cord roots are rich in it. Less than it in the front roots and peripheral nerves.

When applying a substance P on the base of the cantaridine bubble in a dose of 10 -4 g / ml, severe pain occurs. It takes a particularly painful nature when testing purified preparations.

There are many other polypeptides causing pain. These include angiotensin - a substance forming in the action of kidney hormone (renin) on plasma globulins. The cluster properties of angiotensin is weaker than Bradykinina. But, as you know, angiotensin has only side pain. Its main action is an increase in blood pressure. Hormones pituitary glands - oxytocin and vasopressin - also cause pain in very high dilutions. Of the inflammatory exudates, the pain began, which was named leukotoxin. It is close to another substance - necrosin, also possessing algae properties when entering the skin.

This fluent list of the climbing compounds formed in the body is far from full. In the process of metabolism, especially broken, pathological, various chemical compounds occur capable of cause pain.

Experience shows that especially sharp pain is experiencing patients in cases where chemical substances Find B. abdominal cavity. Pump, bile, contents of the stomach and intestines, urine, cavalous masses, in contact with the chemicals of peritoneum, cause heavy pain in the abdomen and diaphragm. This is explained by the sudden, literally unbearable, as if piercing the pain when the contents of the stomach or intestine (for example, when wearing ulcers, with a gallbladder break, with perforative appendicitis) pours abdominal cavity. These pain often end with a shock, cardiac arrest and a sudden death.

When the ulcer of the stomach gastric in the peritoneum is poured a large amount of hydrochloric acid. This can also cause pain shock. The same pain occurs when the bladder breaks, when the satubs are saturated with a solution of urine penetrate into the cavity of the abdomen. And gastric juice, and urine, applied to the base of the cantaridine bubble, cause painful pain. On a scale of Kila, she gets the highest score.

But the diversity of the climbing substances is not at all limited by metabolites formed in the very organism. Each of us experienced pain in the injection of medicinal substances into the skin, in the muscle, even in Vienna. We scream from pain when we bite the wasp or bee, it hurts to us if the nettle burns us.

The clicher substances are contained in poisonous and non-separated discharges of various insects, amphibians, fish, and meanwhile, well-studied chemical compounds of type acetylcholine, histamine, serotonin. In many cases, we experience pain because various enzymes penetrating our body when bitten, contribute to the formation of kinines or other clichery chemical compounds. Sometimes these are oxidases, lipases, dehydrases, breaking tissue breathing. Sometimes toxins resembling bacterial. Sometimes substances overwhelming enzymes. Sometimes paralyzing nervous system poisons.

The bee poison contains not only free histamine in a fairly high concentration, but also substances exempting the associated histamine in the affected fabric of the victim of the attack. Under the influence of the vessels, the vessels are expanding, the permeability increases them, swelling is formed. German scientists Neuman and Gaberman allocated two protein fractions from the bee poison, capable of cause pain. Apparently, they act on free nervous endings and cause the pain characteristic to bite.

The rally poison contains not only histamine, but also serotonin, as well as a substance similar to Bradykinin, called "Osin Kinin". It can cause acute burning pain, but is neither bradykinin nor Callidine.

A huge amount of acetylcholine contains Sherchnya poison. It also detects serotonin, histamine, as well as kinin, differing in their terrific properties from the aspen.

It is interesting to note that snake poisons, especially poison cobra, viper and some other poisonous snakes, do not contain acetylcholine, serotonin or histamine. Snake bite causes instant pain thanks to a large number of potassium and high content in it of the liberators of histamine. But the main terrestrial action snake poison It is associated with the presence of enzymes that implement the formation of kininov from KININOGEN.

The annoying and burning action of nettamine also depends on the presence of histamine, serotonin and some others in it, while there are still few studied substances that contribute to the liberation of histamine from the related form.

Conclusion

Bradykinin, which is one of the mediators of pain, inflammation, plays an important role in increasing the permeability of microscopes. It is he who increases the permeability of the vessels, causing the "opening" of the edges of their endothelium and thus opening the path of blood plasma into the focus of inflammation. His formation is a complex biochemical process, which is based on the interaction of a number of factors. Initially, the process of Hageman's factor is entering the process - an important component of blood coagulation system. Passing a number of consecutive changes, it ultimately turns into Callermine protease, which is cleaved by a biologically active peptide bradykin from a high molecular weight protein. In addition to participating in the formation of Bradykinin, the chageman factor induces the blood coagulation system, which contributes to the insulation of the focus of inflammation, preventing the spread of infection by the body.

Reducing blood pressure is due to bradykinin and acetylcholine. Biogenic amines and bradykinin increase the permeability of the vessels so that during allergies, in many cases, edema develops. Along with the expansion of the vessels, their spasm is observed in some organs. So, in rabbits, the allergic reaction is manifested in the form of a spasm of the vessels of the lungs.

Biologically active amines and kinins under normal conditions are mediators pain sensitivity. They all cause pain, burning, itching when exposed to very small quantities, can affect other nervous receptors in the bloodstream and tissues.

Kinina, serotonin and histamine cause a reduction in the inexharicable muscle bronchi tissue.

Information sources

1. http://oddandeven.narod.ru/nauka_o_boli/ch06.htm.

2. http://gastrosite.solvay-pharma.ru.

3. http://asthmanews.ru/?p\u003d1716

4. http://pathophysiology.dsmu.edu.ua.

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Medicine and veterinary medicine

Inflammation Essence of inflammation Cardinal signs Adaptive role of inflammation Types of local and general processes When inflammation Causes of inflammation Mechanisms of alteration Dynamics of vascular response in the focus of inflammatory Exdation mechanisms Mediators Inflammation of the phagocytosis stage The value of unfinished phagocytosis. Forms of inflammation Alteractive V. Inflammation mechanisms: Alteration: Starting mechanism V. Lizosomes enzymes lead to the degranulation of fat cells and the exit of histamine The most important mediator of inflammation ...

Lecture 4.

INFLAMMATION

Essence of inflammation, cardinal signs, adaptive role of inflammation, types, local and general processes in inflammation, causes of inflammation, alteration mechanisms, vascular dynamics in the focus of inflammation, exudation mechanisms, inflammation mediators, phagocytosis steps, the value of unfinished phagocytosis.

Inflammation - a typical pathological process - an evolutionary formed protective and adaptive response of the body for localization, destruction and removal of a pathogenic agent, characterized by the emergence, exudation and proliferation phenomena. (Vascular reactions and phagocytosis) are isolated separately).

Only in V. There are always all 3 factors - alteration, exudation and proliferation. Evolutionary prototype V. - intracellular digestion (remained as phagocytosis in multicellular).

B. - Adaptive Reaction that eliminates the pathogen agent, but tissue damage in the course of B. Indicates its pathogenic character, which requires control and therapeutic regulation.

Pathogenne - pain, swelling, violation of the function, alteration, exudation with further infection, proliferation - with excess (granules), ischemia, venous hyperemia with thrombosis, increasing the permeability of lysosomes, allocation of histamine, prostaglandins, etc. Bav in excess, physicochemical disorders ( Overlooking, swelling), the predominance of glycolysis and the lack of the Pasteur effect,suppuration (an increase in the alteration, dissemination of infection), amyloidosis in chronic infection, the connecting and wedliness of the scar with the loss of parenchyma, sharp general changes.

Santogenesis C.: Arterial hyperemia - oxygen saturation, venous - focus localization (together with edema, stas and thrombosis), pain - tissue spares, exudation - stimulates phagocytosis, proliferation - healing; Lizosoma - the death of the pathogen agent.

Forms (types) of inflammation - Alteractive V., Exudative B. (serous, fibrinous, purulent, hemorrhagic and frozen - rotten) andProliferative V..

The role of the state of the organism : The severity of V. - from the reactivity of the body (from an- to hyper-ergia).

Cardinal signs W: (Galen and Celsis) 1. Sales (rubor ) - arterial hyperemia (venous - cyanosis), 2.Aripuchness (tumor ) - Tour of the fabrics increased, 3. heat (calor ) - arterial hyperemia, peptide pyrogens and amplification of exchange, 4. Pain (dolor ) - Irritation pain receptors bioactive substances and edema compression, 5. Violation of the function (functio Laesa. ) - pain, edema, alteration, change exchange, etc.

General reactions (System) with V. - Fever (IL-1 and IL-6), leukocytosis (from depot and leukopoietins), increase in ESP (disproteinmeymic, acidosis, hypercalemia, proagrocants, increase adhesion, aggregation of erythrocytes), immune rings and disproteinmes (raising Globulinov), the yield of granulocytes from the depot (bone marrow), hormonal changes (activation of the sympathy-adrenal system, stress), changes in hemostasis, disfermenia.Local reactions - usually withingISTION Fabrics (structural and functional unit - parenchyma, connecting tissue, vessels, nerves).

The reasons B. Exogenous and endogenous. Infectious and non-infectious in nature - mechanical (injuries), physical (heat, UV, cold), chemical, biological (toxins, microorganisms).

Inflammation mechanisms:

Alteration : launcher V., the result of the direct action of the pathogen agent (1-person alteration) and damage to lysosomes, as well as local reflexischemia (2-person alteration) - which leads to a chemically induced increase in vessel permeability, to transudation and exudation. Lizosoma enzymes lead to the degranulation of fat cells and exithistamine (the most important inflammation mediator) - the formation of pores between endothelial cells and intracellular transport channels; Reduction of veins walls on histamine increases pressure and permeability in a microcirculatory bed. Enzymes lysosomes through the chageman factor and with participation -Globulins - formfactor permeability vessels and also activatedkallikrein And the release circuit is launchedkininov (Also increase permeability).

Activated in response to chemical changes systemcomplement - C`- dependent lysis membranes. Phospholipase of lysosomes split phospholipids of cell membranes with arachidonic acid synthesis and inductionprostaglandinov - Mediators inflammation. Lizosoma enzymes are also activated by proliferation processes.

Scheme 1. Inflammation mechanisms (alteration)

Pathogenic alteration (1-person alter. + Reflect. Hyphemia)

agent

Increased penetration Furious cell damage

Tweaks of vessels lysosomes veins and thrombosis

histamine 

Factor Hageman Activation Disorder

+  -Globulins Complementperipheral

  blood circulation

F-P penetrated membranes

Ships and kinines  violated. Emigration exchange

 Phospholipids leukocyte

transudation and exudationPG

Vascular reaction: Primary short-term spasm of vessels leads toischemia fabrics (because Vasoconstrictors are more sensitive to irritation), then vazodilators are excited and developingneuronicarterial hyperemia which is quickly replacedneuroparalytic (and myoparalic) arterial hyperemia, and damage to the walls of the veins and lymphosophose leads to thrombosis andvenous hyperemia, it leads to edema and surveillance from the outside, a closure vicious circle of venous hyperemia.

Ischemia : Seconds, Vasoconstriction - Catecholamines (KA), Thromboxane A2 (TRB2 ), leukotrienes (LT).

Neuronichyperemia : acetylcholine (ah); excess for alteration and ischemia tissue to+ and H + increases sensitivity to it.

Gumoral mechanism : kinines, prostaglandins, adenosine, nitrogen oxide, histamine.

Mioparalyticmechanism : Reducing the basal tone of the arteriole under ischemia and acidosis.

Scheme 2. Inflammation mechanisms (vascular reaction)

Neurogenic  neurotonic-  Neuroparalytic venous

ischemia (ka, kaya hyperemia skia hyperemia hyperemia

Tra 2, Lt) (ah + k +, n + ) + myoparalytic andthrombose

(kinines, PG, adenosine,NO, Histamine)

Exudate : Liquid leaving the microshosuds with large cozy of protein and uniform blood elements.

The reasons : Increased vessel permeability (hydrolysis of basal membrane, reducing actomiosis in endothelium, destruction of the endothelium cytoskeleton, the formation of slot- ischemia, acidosis, alteration)

Leukocyte emigration:after 1-2 hours: Edge standing - adhesion - passage through the wall (3-6 min) - Chemotaxis and electroactsis (H +, Na +, K +, Ca 2+, MG 2+ , protein micelles) - phagocytosis.

Changes in metabolism with inflammation:

Carbohydrated: a sharp increase in energy consumption and blood, damage mitochondria leads to a lack of2 and reduce oxidation processes, sharply activatedglikoliz (with a decrease in ATP and increasing ADP from AMF) and risesdairy Acid, Pirovrobal, etc. (characteristic absence of the effect of pasteur - no oxygen inhibition of anaerobic cleavage of carbohydrates).

Fatty : amplification of lipolysis (release of lysosomal lipases and phospholipas from damaged cells and leukocytes and their activation in an acidic environment) in the focus increases the numberfree fatty acids (LCD) and also perverts exchange with the appearance of localketone tel (CT), the appearance of lipid peroxidation products.FLOOR ), phospholipases activate the formation of arachidonates - inflammation mediators -leukotriene I. prostaglandinov.

Protein: increasing proteolysis , Bioactive educationpeptides, increasing oncotic Pressure - swelling and swelling of the fabric.

Ions and water : Transmembered imbalance: access to+ and Mg 2+ and input to Na + and Ca 2+ cells , breaks out the function and energy of the fabric,hydration Fabrics and violation of cell potential function.

Acidosis : Typical in the focus of C.: Unpainted compounds (lactic acid, higher fatty acids and ketone bodies) due to glycolysis, lipolysis, proteolysis (amino acids); localischemia; stasis blood; Exhausting buffer systems over time.Acidosis leads to: increase the permeability of vessels andedema , increase the permeability of cell membranes andnastya Fabrics, enzyme activationlizosoma, pain , Changes the sensitivity to bioactive substances and their effects (the sensitivity to adrenomimetics is reduced and increases to cholinomimetics), protein hydrolysis - hyperoncia - swelling, increase in hydrolysis of various substances - hyperosmia - swelling.Hyperosmia : Increased proteolysis, macromolecules hydrolysis, cell decay.Leads to : Heal hyperhydration, increase the permeability of vessels, stimulation of leukocyte migration (chemotaxis), changing the tone of vessels, pain.

Hyperonkia. : Enzymatic and non-enzymatic hydrolysis of proteins, change in the conformation of proteins and micelles with an increase in hydrophilicity when the ions are attached in the focus of inflammation, the output of albumin from vessels.Leads to: edema in the hearth.

Physics and chemical reactions : Dairy and fatty acidsscrew the hearth at.: Primary acidosis as a result of ischemia, then with arterial hyperemia - longmetabolic acidosis Initially compensated and then decompensated. Protelyolis enhancesoncotic local pressure; lysis and necrosis lead to an increaseosmotic Pressure and output intracellular to+ it leads to an increase in the turgora andfabric edema.

Scheme 3. Inflammation mechanisms (exchange violations)

Carbohydrates: Glycolizis Acidosis lactic acid

Fats: LCD and CT, Paul, PG and LT

Proteins: Protelysis Bav (peptides) and hyperonkia

Ions, water: yield K + and MG 2+ Entrance to the Na + and Ca 2+ cell  hyperosmia

In the fabric observed:

Acidosis: as a result : ischemia, stas, metabolism (lactat), lysosomes

Leads : edema, swelling, pain, hyperonkia, hyperosmia, perversion.

Hyperonkia: Due to : proteins hydrolysis, albumin output

leads To: swelling in the focus of inflammation

Hyperosmia: as a result : Proteoliz and protein hydrolysis, lysis CL.

leads To: Hypermigrastation, Lukucet Migration, Transudation, Pain

Bioactive substances at V. (Mediators B.): Change the exchange, local vascular reaction, lead to alteration, increase vascular permeability, stimulate proliferation. It:

lysosomal enzymes (hydrolase and lipase, phospholipase);

prostaglandins (Phospholipase A + phospholipids membranes - arachidon K-Ta - cyclooxygenase - prostaglandins) - accelerate the bloodstream, increase the permeability of tissues and emigration of leukocytes, participate in the development of fever, increase the effect of bradykinin on the vessels; Through cyclic nucleotides, the intensity is regulated. :( PGE - CAMF - Reduces PGF - TsGMF - Raises V.);

lakeotrienes : Long-term reduction in smooth muscle cells leads to ischemia, mambrane labilization with lysosomes and increases V.

Group of active peptides : cause an increase in temperature, necrosis, leukocytosis, proliferation stimulation.

Cytokines : Interleukin-1-4, 6 and 8 - stimulate chemotaxis phagocytes, synthesis of prostaglandins, adhesion endotheliocytes, stimulate proliferation, microtromes and febride.

Spicy phase proteins - stimulate chemotaxis and the yield of granulocytes from the bone marrow.

Cationic proteins : from granulocytes, nonspecific bactericidal activity, stimulation of leukocyte emigration, increase the permeability of vessels.

Fibronctins : Synthesis by many cells - SPEOsonize phagocytosis objects and activate hemotaxis leukocytes.

N Easerediators: adrenaline and norepinephrine (activation of glycolysis, lipolysis, lipoperoxidation - floor, spasm arteriole - ischemia),acetylcholine (decrease in tone arterioles - hyperemia, leukocyte emigration, cell proliferation).

Biogenic amines: Histamine (from fat cells - pain, burning, increase in the permeability of vessels, migration of cells) andserotonin (from platelets and fat cells - pain, increasing vessel permeability, reducing veins - venous hyperemia, promotes thrombosis).

Azota oxide (Synthesis of endothelium - normal vasidation). ProductsFLOOR -Beclotable and radical and lipid peroxidation and n2 O 2. - Toxic and regulatory effects.

Nucleotides and nucleosides (ADF, adenosine): ADP stimulates adhesion, aggregation and agglutination - thrombosis, sweet, stas, ischemia (in venules - hyperemia).

Plasma Mediators: Kinina (Callidin, Bradykin) - an increase in vessel permeability is stronger than histamine, edema potentiation, leukocyte emigration;complement factors- chemotaxis, opsonization, cytolysis, bactericidal effect, regulation of the synthesis of kinines and immunity and hemostasis;coagulation system (pro- and anti-coagulants, fibrinolities) - the result of damage to the walls of the vessels; leads to: thrombosis and stas, ischemia, venous hyperemia.

PHAGOCYTOSIS : Absorption and digestion of corpuscular particles (foreign ongredients - initially or becoming such).

Main types of cells -neutrophilic polymorphonuclars.

The most important normal phagocytosis mechanisms: polymerization -Epolymerization of microtubules of the cytoskeleton under the action of CAMF-CGMF and Ca2+ lead to pinocytosis and secondary phagelicosums.

Stages: 1st - adhesion to endothelium (When damaged), the formation of pseudopodies and penetration between endothelial cells, lysis of the basal membrane of a vessel with collagenase and the yield of phagocyte into the fabric.

2nd - Chemotaxis To the facility of phagocytosis: positive chemotaxis - on polypeptides, etc. TsGMF strengthens, the CAMF suppresses it. During the movement, changes in the cytoplasm of the type of gel-sol - in the front of the phagocyte and the flow of a cortical gel on microtubule; Aktin-myosine contractile filaments also apply. F. - Energy-dependent (Glycolizis mainly).

3rd: sticking to paragocyattedagent - from electrical charges of fabric and phagocyte, etc.

4th - Dive agent in phagocyte (shell invagination) - from electrical charges and surface tension, antibodies -opSonins.

5th: digestion : In the digestive vacuole, the pH shift and draining with lysosomes, a metabolic explosion - AFC. Possible and emission of granules from phagocyte outwards.

Integrated phagocytosis - microorganisms with a polysaccharide capsule, leads to chronic infection (for example).

PROLIFERATION : Increased stroma, often parenchyma (regeneration) and intercellular substance in the V. Focus, promotes regeneration and healing after alteration. Good regeneration: liver, leather, mucous, bone); Weak: tendons, bundles, cartilage; no regeneration: myocytes, neurons - are replaced by connect fabric (scar).Activation P. - with a decrease in inflammation: inhibitors of proteases, antioxidants, polyamines, glucocortcides, heparin.

Regulators P.: Mediators inflammation (tumor necrosis factor, leukotrienes, kinins, biogenic amines); lymphokins, growth factors (including platelets); polyamines; Hormones (STS, insulin, glucagon, steroids), venous hyperemia stimulates the healing of the fabric.

Chronic inflammation : 1-way (immediately) and 2-way (ploking).Manifestation: Granulomas (tuberculosis, brucellosis),infiltration Mononucleases of the hearth V., formation of fibrouscapsules and calcification, necrosis In the center of the hearth V.

The reasons : Fogocytosis deficiency, long-term stress (catecholamines and glucocorticoids), repeated tissue damage, persistent infection, autoimmune aggression.

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