From Big Medical Encyclopedia

INFLAMMATION — composite, complex local vascular and fabric (mesenchymal) zashchitnoprisposobitelny reaction of a complete organism on action of a pathogenic irritant. This reaction is shown by development on site of damage of fabric or body of changes of blood circulation is preferential in a microcirculator bed, increase in permeability of vessels in combination with dystrophy of fabrics and proliferation of cells.

The general pathology

Short historical data and theories

the big place in medicine was always allocated to the Question of value and V.'s essence. Still Hippocrates considered that V. has the neutralizing value for an organism that in a suppurative focus the harmful beginnings are destroyed and therefore formation of pus is useful, salutary if a certain limit of intensity of inflammatory process is only not exceeded. Hippocrates's views of V.'s nature dominated up to 18 century, being supplemented with the description of «cardinal signs» of an inflammation.

A. Tsels the wedge, V.'s sign described four main: redness (rubor), swelling (tumor), pain (dolor), temperature increase (calor). The fifth sign — dysfunction (functio laesa) K. Galen described; he spoke about an inflammation as about local fever and pointed to a variety etiol, factors, to-rye it can cause.

The first idea, close to modern, of V. was formulated by the English surgeon J. Gunter, to-ry defined V. as reaction of an organism to any damage. Gunter considered V. the protective process always arising on site damages, with the help to-rogo normal function of the damaged fabric or body is recovered.

The doctrine about V. began to develop after improvement of a light microscope (the middle of 19 century), and also in the first half of 20 century in connection with development biochemical, biophysical, and gistokhy. methods and methods of elektronnomikroskopichesky studying of fabrics. R. Virkhov (1859) paid attention to damage of a parenchyma of bodies (dystrophic changes of cells) at V. and created the so-called nutritive («nutritious») theory of B. This theory lost value in connection with Samuel's researches (S. Samuel, 1873) and Yu. Kongeyma (1887), to-rye major importance in V.'s pathogeny reactions of small vessels (the vascular theory of V.) gave.

A.S. Shklyarevsky (1869) applied an experimental method to studying of a blood-groove at V. and gave physical. explanation for a phenomenon of «regional standing of leukocytes». A. G. Mamurovsky (1886) noted thrombosis and blockade limf, vessels in V.

Osobenno's center the big contribution to development of a problem B. was made by I. I. Mechnikov, to-ry in 1892 formulated the biological theory of V., developed the doctrine about phagocytosis (see), laid the foundation for comparative pathology of V. and the theory cellular and humoral immunity (see). Process of absorption by phagocytes of foreign debris, including bacteria, was recognized by I. I. Mechnikov the basic, central process characterizing V. V the lectures on comparative pathology of an inflammation I. I. Mechnikov wrote about process of the intracellular digestion which is carried out in cytoplasm of phagocytes.

Development of the idea of I. I. Mechnikov about value of phagocytosis for protection of an organism against a pathogenic factor and formation of immunity was received in works of H. N. Anichkov, A. D. Ado, Kohn (E. J. Cohn, 1892 — 1953) and many other scientists. With opening in 1955 of cytoplasmatic organellas — lysosomes (see) — I. I. Mechnikov's doctrine about cytoses as carriers of the digesting function of a cell received further confirmation.

V. V. Voronin in 1897 established value of a condition of interstitial fabric and a tone of vessels at V. Otvodya to process of phagocytosis a supporting role, the main mechanisms which are the cornerstone of V., he considered the processes happening in interstitial substance of connecting fabric and gave the interpretation of the phenomenon of emigration, wandering of cells and phagocytosis differing from mechnikovsky. Voronin's theory did not open biol, entities of an inflammation. V. V. Podvysotsky in «Bases of the general and experimental pathology» (1899) wrote that at V. discrepancy of endothelial cells is observed owing to what between them openings are formed, through to-rye leukocytes get from a vessel into perivascular space.

In 1923 H. Schade put forward physical. - the chemical theory of V.: in his opinion, V.'s basis is the tissue acidosis, the Crimea and all set of changes is defined. Rikker (G. Ricker, 1924) considered V.'s phenomena as manifestation of neurovascular frustration (the neurovascular theory of V.).

For clarification of a histogenesis of V., a role of the cellular forms participating in inflammatory reaction A. A. Maximov's works had great value (1916, 1927),

I. I. Mechnikov gave A. A. Zavarzin (1950) and other scientists who created pilot models of V. and studying transformation of cellular forms in V.'s center === Comparative pathology === the Classical description of comparative pathology of V., having shown that V. always represents active reaction of an organism, at whatever step of evolutionary development it was. I. I. Mechnikov tracked development of all phases of inflammatory reaction at different stages of phylogenesis — alteration, exudation and proliferation, phagocytosis in detail described; at high-organized animals assigned a big part in phagocytosis to neuroregulatory mechanisms. An organism, I. I. Mechnikov specifies, it is protected by means, to-rymi has. Even the elementary unicells do not belong passively to harmful irritants, and fight with them by phagocytosis and the digesting effect of cytoplasm. However and the elementary unicells at influence of a pathogenic factor have phenomena of alteration similar a nek-eye to dystrophic processes in metaphytes. At metaphytes reaction to damage becomes complicated due to proliferation of cells and the created vascular system; the organism can already «send» considerable number of phagocytes to the place of damage. At later stages of phylogenesis organisms have an emigration of cells. With formation organisms of endocrine and nervous systems have neurohumoral factors of regulation of inflammatory reaction.

At high-organized animals other protective and adaptive processes join phagocytosis: blockade venous and limf, the vessels which are taking away from V.'s center, exudation of the serous liquid liquefying toxic products, antibody formation the proliferating plasmocytes neutralizing a pathogenic factor.

The data on phases B. received during the studying of inflammatory reaction in phylogenesis show its complication in process of evolution of organisms; phases B. to a certain extent repeat in the prenatal period of the person. Yu. V. Gulkevich (1973) showed that the germ has considerably smaller reactivity in comparison with an adult organism and at the earliest stages of development the embryo reacts to harmful effects only death, however at early stages of development also proliferation of cells can already be observed. Exudation with existence of leukocytes is found in a fetal part of a placenta and a fetal membrane already to 10 — 12 weeks and is the latest ontogenetic component of inflammatory reaction. Phagocytosis at a germ of the person is carried out by hl. obr. macrophages of connecting fabric, and is later segmentoyaderny granulocytes.

Development of inflammatory reaction in ontogenesis of the person is closely connected with formation immunol, reactivity that is morphologically expressed by emergence of a large number of the plasmocytes producing immunoglobulins, number to-rykh much increases at emergence in an organism of a germ of inflammatory focus. Researches show that inflammatory reaction with existence of all signs of V. is established on 4 — the 5th month of an antenatal life of the person. In the post-natal period at V. impact on an organism of antigenic irritants of the environment and immunol amplifies, processes in a bigger degree complicate kliniko-morfol. a profile B.

the Aetiology and pathogenetic mechanisms

the Reasons of an inflammation can be diverse: biol., physical., chemical, mechanical, both an exogenous, and endogenous origin. V.'s development is defined not only etiol, a factor, but also reactivity of an organism (see). So, nek-ry even fiziol, irritants, own excretes, at change of localization of action or during the weakening of an organism can cause Century. Among biol, V.'s reasons the most frequent are microorganisms: staphylococcus, streptococci, pneumococci, colibacillus, rickettsiae, pathogenic fungi, and also zooparasites. To exogenous physical. and to chemical factors of V. refer radiation, a burn, a frostbite, injuries, influence of chemical substances (e.g., strong to - you, alkalis, turpentine, croton oil). Endogenous chemical substances cause inflammatory reaction in the place of their allocation; e.g., at uraemia uraemic toxin causes a coloenteritis, a pericardis, etc. V. can develop around foreign bodys, infarctions of fabrics; in these cases it as if delimits a foreign body or the center of a necrosis from surrounding living tissue and therefore is called a demarcation (restrictive) inflammation.

Inflammatory reaction consists of several phases interconnected among themselves: a) alterations of fabrics and the cells making them; b) release of physiologically active agents (so-called mediators of V.) that makes triggers B. and involves reaction of vessels of microcirculation; c) increases in permeability of walls of capillaries and venules; d) reactions of system of blood to damage, including changes of rheological properties of blood (see. Blood , Rheology ); e) — a reparative stage

of V. V the practical purposes it is reasonable to proliferation to divide conditionally three main interconnected among themselves a component B., having bright kliniko-morfol. expression: alteration with allocation of mediators, vascular reaction with exudation and proliferation. Classification of the main morfol, forms B. is based on dominance of this or that of these components.

Alteration (damage of fabric and cells) it is possible to consider as result of direct action of a pathogenic factor and the exchange disturbances arising in the damaged fabric. It is the first phase B.; it characterizes initial processes and is morphologically shown from scarcely noticeable structurally functional disturbances before full destruction and death (a necrobiosis, a necrosis) of fabrics and cells (see. Alteration ). Alterativny changes at V. are especially brightly expressed in the high-differentiated fabrics performing difficult functions, napr in neurons; in the fabrics which are carrying out hl. obr. basic function and making a stroma of body, napr, in connecting fabric, alterativny changes often come to light hardly. In parenchymatous bodies alteration is shown by different types proteinaceous dystrophy (see) and fatty dystrophy (see), in their stroma there can be a Mucoid and fibrinoid swelling up to a fibrinoid necrosis (see. Fibrinoid transformation ).

In c. the N of page alteration is expressed by change of ganglionic cells (neurocytes) as a lysis of basphilic (tigroid) substance, a pushing off of kernels to the periphery and pycnosis (see), swellings or wrinklings of cells. In mucous membranes alteration is expressed by damage of an epithelium, desquamation (see) with an exposure of a basal membrane; mucous glands strenuously emit slime, to a cut the desquamated epithelium is added, gleams of glands extend (see. Mucous dystrophy ).

Ultrastructural changes at V. happen both in components of cytoplasm, and in a kernel of a cell and its membrane. Mitochondrions increase in sizes, bulk up; nek-ry mitochondrions, on the contrary, shrivel, cristas collapse; the form and size of tanks changes endoplasmic reticulum (see), there are vesicles, concentric structures, etc. Change as well ribosomes (see). In a kernel of a cell damage is shown by a regional arrangement of chromatin, ruptures of a membrane of a kernel.

In many cases alteration develops by means of so-called lysosomic effect: at destruction of membranes lysosomes (see) the enzymes playing a significant role in damage of structures of cells are released various, especially hydrolytic.

Mediators of an inflammation — a number of physiologically active agents considered as triggers B. under influence to-rykh arises a fundamental unit of V. — reaction of vessels of a microcirculator bed and the proceeding blood with disturbance of rheological properties of blood that makes an initial phase of inflammatory reaction. V.'s mediators promote increase in permeability of vessels of microcirculator system, its especially venulyarny department, with the subsequent exudation of plasma proteins, emigration of all types of leukocytes, and also erythrocytes through walls of these vessels. These physiologically active agents play an important role in V.'s manifestations, and nek-ry researchers call them «internal engines»

V. Spector and Uillobi (W. G. Spector, D. A. Willoughby, 1968) provide 25 names of physiologically active agents (chemical mediators) of a different action spectrum appearing after damage of fabric. Especially many works about V.'s mediators appeared after opening of a histamine and leukotaxine. Though leukotaxine in the subsequent test works was substance of the heterogeneous nature, its studying served as an incentive for further researches of endogenous chemical mediators of V., the most important of to-rykh is considered to be a histamine, serotonin, plasma kinina, RNA and DNA decomposition products, hyaluronidase, prostaglandins, etc.

One of the main sources of chemical mediators of V. are mast cells (see), in granules to-rykh the histamine, serotonin, heparin, etc. is found; in cytoplasm of mast cells cytochrome oxydase, acid and alkaline phosphatases, enzymes for synthesis of nucleotides, proteases, eksteraza, a leucine aminopeptidase, plasmin are found.

Spector and Uillobi most convincingly showed especially important role histamine (see) in releasers V. Gistamin is the first vasoactive substance appearing at once after damage of fabric; starting stages of a vazodilatation, increase in vascular permeability and exudation are connected with it; the histamine has preferential effect on venules. Is also of great importance serotonin (see).

On microcirculation (see) at V. exert impact catecholamines (see) and kinina (see). As kinina are regulators of a tone of a vascular wall and cause expansion of a gleam of arterioles and increase in permeability of venules, their role in development V. is quite considerable, especially bradikinin (see. Mediators of allergic reactions ).

Among V.'s mediators it should be noted a globulinovy factor of permeability (PF/dil.), opened in a blood plasma of a Guinea pig by A. A. Miles with sotr. (1953, 1955) and T. S. Paskhina (1953, 1955) in aseptic inflammatory exudate, blood serum of a rabbit, dog and the person; this factor promotes release of bradikinin by means of kallikrein. Spector believes that the globulinovy factor of permeability has close connection with the mechanism of a blood coagulation, and in particular with Hageman's factor (see. Coagulant system of blood ). According to Myles, Hageman's factor is activated by the predecessor of PF/dil globulin., active PF/dil is formed., and the chain of consecutive reactions joins further: a prekininogenaza — a kininogenaza — kallikrein — kininogen — kinin.

Nek-ry nucleosides take part in inflammatory reaction; adenosine can cause increase in permeability of walls of microvessels and local accumulation of leukocytes; nek-ry nucleosides are the liberator (releasing) of a histamine.

Vascular reaction with exudation plays very large role in mechanisms B. A number of authors claims that all «an appearance of an inflammation», all its features, all scale of fabric changes are defined by vascular reaction, permeability of vessels of a microcirculator bed, weight of its damage.

In the earliest phases B. activation of functions of an endothelium of capillaries is noted. In cytoplasm of an endothelium the number of microvesicles increases, there are accumulations of cytogranules, polyribosomes are formed, mitochondrions bulk up, cavities of an endoplasmic reticulum extend. Endothelial cells change the configuration a little, bulk up, their membranes become friable (see. Permeability ).

Mechanisms of passing of substances of various molecular weight and blood cells through an endothelial vystilka and a basal membrane of capillaries and venules long remained not clear. Using methods of a submicroscopy it is established that endothelial cells in capillaries with a continuous endothelium, closely adjoining to each other, only in certain places are linked among themselves to the help of desmosomes (tight joints). The cell on a basal membrane is strengthened and fastened to the next cells colloid weight like proteinat of calcium in combination with mucopolysaccharides. In patol, conditions the body of a cell can be reduced, change the form and move. The complex of the endothelial cells covering an inner surface of vessels of microcirculation is a mobile system, during the functioning a cut in intervals between endothelial cells there can be cracks, and in a body of cells — even channels. Interendothelial cracks should be carried to a so-called small time, and channels in a body of an endothelial cell (microvesicular transport) — by a so-called big time, through to-rye and transcapillary transport is carried out. Dynamic elektronnomikroskopichesky observations

And. M. A seamy side with sotr. showed that, napr, at pneumonia, microvesiculation of an endothelium of capillaries and formation of larger endothelial microbubbles considerably amplifies that indicates increase in fabric exchange.

In V.'s center there are expressed frustration of a blood-groove and a lymphokinesis. After damage of fabric by the earliest change at acute inflammatory reaction reduction of arterioles is quickly passing (of 10 — 20 sec. to several minutes). Most of researchers does not attach great value to this phenomenon, however Spector and Uillobi consider it the defense reaction caused by catecholamines. Soon two phases of vasodilatation develop. The first phase (an immediate vazodilatation) which is followed by increase in permeability in relation to blood proteins reaches a maximum on average in 10 min.; the second phase, much longer, is measured several hours. Owing to the second phase of vasodilatation there is an infiltration of fabrics leukocytes, inflammatory hyperemia (see), rheological properties of blood change, there are staza, local hemorrhages, thrombosis of small vessels; in V.'s center the metabolism amplifies, to-ry it is expressed by strengthening of hydrogen ions, acidosis, a hyperosmia. In limf, microvessels develop a lymphostasis and limfotromboz.

Shifts of rheological properties of blood begin with change of speed of a blood flow, disturbance of axial current, a vykhozhdeniye from it white blood cells and their arrangement along walls of post-capillary venules (so-called regional standing of leukocytes); units of thrombocytes and erythrocytes, staz and thrombosis of venules and capillaries are formed. Thrombosis arises in connection with activation of a factor of Hageman, an important component of coagulant system of blood. Then occurs exudation (see), i.e. a vykhozhdeniye from vessels in fabric of components of blood — water, proteins, salts and blood cells. In V.'s center find the metabolic products, toxins which came out a blood flow, i.e. V.'s focus performs as if drainage eliminativny function. The Ekssudirovavshy or entered directly into the center by V. substances (e.g., paints) are removed poorly owing to thrombosing venous and limf, vessels in the inflamed fabrics.

Exudation of proteins occurs in the sequence, edges is explained by the size of molecules (the smallest molecule of albumine, the largest — fibrinogen): at small extent of increase in permeability albumine, in process of increase in permeability — globulins and fibrinogen is emitted. Exudation of proteinaceous molecules occurs hl. obr. via channels in a body of an endothelial cell (a big time) and to a lesser extent through cracks between endothelial cells (a small time).

Vykhozhdeniya from a blood flow through a wall of venules and capillaries of cellular elements of blood, hl. obr. leukocytes (segmentoyaderny granulocytes and monocytes), regional standing of leukocytes, their gluing to a vascular wall precedes. A.S. Shklyarevsky (1869) showed that the vykhozhdeniye of leukocytes from axial current is in full accordance with physical. the law of behavior of the particles weighed in fluxion at delay of speed of its movement. After gluing to endothelial cells segmentoyaderny granulocytes form the pseudopodiums getting through a vascular wall, contents of a cell are poured towards the leg extended out of limits of a vessel, and the leukocyte appears out of a vessel. In okolososudisty fabric segmentoyaderny granulocytes continue the movement and are added to exudate.

Process of emigration of leukocytes is called a leukodiapedesis. It is established that emigration of segmentoyaderny granulocytes and mononuclear cells is a little various. So, segmentoyaderny granulocytes (neutrophils, eosinophils and basophiles) will emigrate between endothelial cells (mezhendotelialno), and agranulocytes (big and small lymphocytes and monocytes) — through cytoplasm of an endothelial cell (transendotelialno).

Fig. 1. Interendothelial emigration of leukocytes through a vascular wall at an inflammation: and — segmentoyaderny granulocytes (1) got into space under an endothelial cell and are located between an endothelium (2) and a basal membrane (3). Joints of endothelial cells (4), collagenic fibers (5), kernels of granulocytes are visible (6); x 20 000; — two segmentoyaderny granulocytes (1) are in perivascular connecting fabric (the basal membrane was recovered in dense gel). The endothelium (2) is not changed, joints (4) of its cells and collagenic fibers of perivascular connecting fabric (5) are visible; gleam of a vessel (7); x 12 000.

Interendothelial emigration happens as follows. In the most initial phase B. the segmentoyaderny granulocyte is pasted to an endothelial cell and between it and the leukocyte as if stretches threads. Then there occurs reduction of an endothelial cell and in the crack formed between two cells pseudopodiums direct; with their help the segmentoyaderny granulocyte quickly enough gets into space under an endothelial cell, edges as if exfoliates, and the opening over it becomes isolated the cells of an endothelium connecting again — the segmentoyaderny granulocyte appears between an endothelium and a basal membrane (fig. 1, a). The following barrier — a basal membrane — the segmentoyaderny granulocyte overcomes, apparently, on the mechanism of a thixotropy (isothermal reversible reduction of viscosity of colloid solution), i.e. transition of gel of a membrane to sol at an insignificant touch of a granulocyte to a membrane. The granulocyte easily overcomes sol, it appears in fabric outside a vessel (fig. 1, b), and the basal membrane is again recovered in dense gel.

At transendothelial emigration agranulocytes are originally pasted to an endothelial cell, activity a cut at the same time sharply increases; the finger-shaped shoots arising at a membrane of an endothelial cell as if take a mononuclear cell from all directions, absorb it by formation of a big vacuole and throw out on a basal membrane. Then on the mechanism of a thixotropy Mononuclear cells get through a basal membrane into perivascular space and are added to exudate.

At V. in fabric leave vessels as well erythrocytes (see. Emigration ). They pass a vascular wall passively at sharp increase in vascular permeability that is observed at highly toxic infections (plague, a malignant anthrax), defeat of walls of vessels by a tumor, a radial illness, etc.

I. I. Mechnikov explained escaping of a vessel of segmentoyaderny granulocytes and advance in the direction to the center of damage with a chemotaxis, i.e. action on leukocytes of the substances which caused V. or formed in V.'s center (see. Taxis ). Menkin (V. Menkin, 1937) emitted the so-called leukotaxine causing a positive chemotaxis of segmentoyaderny granulocytes from inflammatory fabric; the positive chemotaxis is more expressed at segmentoyaderny granulocytes, less — at agranulocytes.

The most important phenomenon of V. is phagocytosis (see), carried out by cells — phagocytes; carry segmentoyaderny granulocytes to them — microphages and agranulocytes — macrophages (see), in cytoplasm to-rykh process of intracellular digestion is carried out. The positive role in processes of phagocytosis of ions of aluminum, chrome, iron and calcium is revealed, opsonins (see).

It is established that various particles and bacteria invaginate a cover of a phagocyte; in cytoplasm of a phagocyte the invaginated part of a cover with the material concluded in it is chipped off, forming a vacuole, or a phagosoma. At merge of a phagosoma to a lysosome the phagolysosome (a secondary lysosome) forms, edges by means of acid hydrolases are carried out by intracellular digestion. At the time of phagocytosis activity of lysosomic proteolytic enzymes, especially acid phosphatase, a collagenase, cathepsines, arylsulphatases A and B, etc. sharply increases. Thanks to the same enzymes the died fabrics are split; removal of decomposition products comes from V.'s center by phagocytosis.

By means of the phenomena of a pinocytic there is an absorption of droplets of liquid and macromolecules, napr, ferritin, protein, antigen (see. Pinotsitoz ). Nossel (G. Nossal, 1966) showed that antigen of salmonellas, marked a radioiodine and entered into an organism of a rabbit, is absorbed by macrophages as a mikropinotsitoz. Molecules of antigen in cytoplasm of a macrophage are affected by lysosomic hydrolases that leads to release of antigenic determinants. The last kompleksirutsya with RNA of macrophages, and then information on antigen is transferred to lymphocytes, to-rye are transformed to the plasmocytes forming antibodies. So, intracellular digestion of antigen comes to the end with immunogene process (see. Immunomorphology ), protective and immunogene function of inflammatory reaction is also carried out, in process the cut arises cellular and humoral immunity.

However along with complete phagocytosis in macrophages it is observed, napr, at nek-ry infections, phagocytosis incomplete, or endotsitobioz when fagotsitirovanny bacteria or viruses are not exposed to full digestion, and sometimes even begin to breed in cytoplasm of a cell. Endotsitobioz explain with a lack or even absence of lysosomes of macrophages of antibacterial cationic proteins what reduces the digesting ability of lysosomic enzymes.

As a result of changes of microcirculation, increase in vascular permeability and the exudation of plasma proteins following it, water, salts and emigration of blood cells in fabrics liquid muddy, rich with protein (from 3 to 8%) is formed — exudate (see). Exudate can collect in serous cavities, between fibrous structures of a stroma of body, in hypodermic cellulose that leads to increase in volume of the inflamed fabric. Exudate consists of a liquid part and cellular weight, contains products of fabric disintegration. Character of exudate does not happen homogeneous: at small degree of permeability of vessels in exudate albumine prevails, it is a little cells, at considerable permeability — globulin, fibrin, it is a lot of cells.

At all types of exudate great diagnostic value has structure of cellular elements since it is not identical at various diseases. So, in purulent exudate neutrophils prevail, at allergic and parasitic V. — eosinophils; dominance of lymphocytes is characteristic for hron. Century, napr, at tuberculosis in exudate (serous pleurisy) lymphocytes and monocytes prevail. In serous cavities to exudate desquamated mesothelial cells, and on mucous membranes — desquamated cells of an epithelium are added. The cells which are in composition of exudate can have hematogenous (emigrated from a blood flow) and gistiogenny, local fabric, an origin.

Dynamics of cellular changes of exudate shows that under the influence of treatment the number of neutrophils originally decreases, and the number of monocytes increases, appears a large number of macrophages. Change in exudate of segmentoyaderny granulocytes with agranulocytes is considered a favorable predictive sign.

Proliferation (reproduction) of cells is the completing, reparative phase B. Reproduction of cells happens hl. obr. at the expense of mesenchymal elements of a stroma, and also elements of a parenchyma of bodies. Stem cells of connecting fabric — polyblasts, or lymphoid cells, adventitious and endothelial cells of small vessels, reticular macrophages limf, nodes, small and big lymphoblasts breed (see. Granulyatsionnaya fabric , Connecting fabric ). At their differentiation in V.'s center mature and specialized cells appear: fibroblasts, fibrocytes, corpulent and plasmocytes, to-rye are differentiated from the predecessors — plasmablasts and big and small lymphocytes; there are new capillaries. At proliferation (see) it is observed as well exudation of neutrophilic, eosinophilic, basphilic leukocytes and lymphocytes, etc.; in this regard distinguish lymphoid, plazmokletochny, eosinophilic and other infiltrates.

Cellular elements in the inflammatory center are exposed to processes of transformation. The Segmentoyaderny granulocytes which executed the phagocytal function quickly enough perish. Lymphocytes a part perish, are transformed by a part to plasmocytes, to-rye gradually perish, leaving a product of the secretion — hyaline spheres. Mast cells perish, the monocytes of blood which got to fabrics become the macrophages who are clearing away V.'s center from a cellular detritis and are carried away by current of a lymph in regional limf, nodes where also perish. Polyblasts and products of their differentiation — epithelial cells, fibroblasts and fibrocytes remain the most resistant cellular forms in the inflammatory center. Sometimes there are multi-core colossal cells arising from epithelial and proliferating endothelial cells. With participation of fibroblasts there is an active synthesis of collagen. Cytoplasm of fibroblasts becomes pironinofilny, i.e. is enriched with the ribonucleoproteins forming a matrix for collagen. V. comes to the end with formation of mature fibrous connecting fabric.

The exchange disturbances arising in V.'s center on Lindnera (J. Lindner, 1966), can be subdivided into catabolic and anabolic processes.

Catabolic processes are shown by disturbances fiziol, balances of the main substance of connecting fabric: processes of a depolymerization proteinaceous mukopolisakharidnykh complexes, formation of decomposition products, emergence of free amino acids, uranium to - t (that leads to acidosis), aminosugars, polypeptides, low-molecular polysaccharides are observed. Such disorganization of interstitial substance increases vascular and fabric permeability, exudation; it is followed by adjournment of blood proteins, including fibrinogen, between collagenic fibrilla and protofibrils that promotes, in turn, change of properties of kollagen.

Defense reactions of an organism considerably are defined by anabolic processes and degree of their intensity. These processes at V. are expressed by increase in synthesis of RNA and DNA, synthesis of the main interstitial substance and cellular enzymes, including hydrolytic. Gistokhim. the researches conducted by Lindner on studying of enzymes in cells in V.'s center showed that especially big enzymatic activity from the moment of emergence in V.'s center is shown by monocytes, macrophages, colossal cells, segmentoyaderny granulocytes. Activity of enzymes of the hydrolases which are markers of lysosomes that allows to assume increase in activity of lysosomes in V. V center fibroblasts granulocytes amplifies activity of oxidation-reduction enzymes increases thanks to what the interfaced process of tissue respiration and oxidizing phosphorylation amplifies.

Early emergence of the cells rich with hydrolases (lysosomes), and first of all segmentoyaderny granulocytes, it is possible to consider as one of manifestations of catabolic processes due to the need of the increased processing of decomposition products; at the same time it promotes anabolic processes.

Factors of regulation and a current

V. is considered as local fabric reaction, at the same time its emergence and a current considerably are defined by the general condition of an organism. The general principle of self-control with a feed-back of information is presented already at the level of a cell. However adaptive reactions within a cell have independent value until the functional systems of all organism reflecting a difficult complex of self-control of cells and bodies keep rather stable state. At disturbance of this state the adaptive and compensatory mechanisms representing composite neurohumoral reactions turn on. It should be meant in the analysis of local features of development of the center of Century.

Both hormonal, and nervous factors can influence V.'s character. Of very great importance nek-ry hormones, hl are for inflammatory reaction. obr. hormones of bark of an adrenal gland and hypophysis that is convincingly shown in an experiment and in clinic by the Canadian pathologist G. Selye. It is established that somatotropic hormone of a hypophysis Desoxycorticosteronacetatum and Aldosteronum are capable to increase inflammatory «potential» of an organism, i.e. to strengthen V. though in itself cannot cause it. Mineralokortikoida, influencing electrolytic composition of fabrics, have pro-inflammatory effect (activate V.). Along with it glucocorticoids (a hydrocortisone and others), adrenocorticotropic hormone, without having bactericidal properties, have antiinflammatory effect, reducing inflammatory reaction. A cortisone, detaining development of the most precursory symptoms of V. (a hyperemia, exudation, emigration of cells), interferes with developing of hypostasis; widely use this property of a cortisone in applied medicine. The cortisone deprives connecting tissue of predecessors of mast cells (big lymphocytes and polyblasts), in this regard there is depletion of connecting fabric mast cells. Perhaps, antiinflammatory action of a cortisone since in the absence of mast cells activity of starting factors of V., napr, the histamine which is formed of granules of mast cells considerably decreases is based on it.

Influence of nervous factors on V. is studied insufficiently. However it is known that at disturbance of a peripheral innervation, especially sensitive, V. gains sluggish, long character. E.g., the trophic ulcers of extremities arising at wounds of a spinal cord or a sciatic nerve heal is very long. This results from the fact that in the fabrics deprived of a sensitive innervation exchange processes are broken, alterativny changes amplify, vascular permeability increases and hypostasis accrues.

The wedge, V.'s current depends on a set of factors. The condition of reactive readiness of an organism, degree of its sensitization is of especially great importance for V.'s current. In one cases, especially at hypersensitivity, V. proceeds sharply, in others — accepts a long current, gaining character subacute or chronic. Also the wavy current of V. when the periods of a zatikhaniye of process alternate with aggravations is observed; flashes of inflammatory process for a row of years, napr are possible, at a brucellosis, tuberculosis, collagenic diseases. In these cases during a disease the period (phase) of immediate hypersensitivity is replaced by the period of hypersensitivity of the slowed-down type. In phases of hypersensitivity exudative and even necrotic changes with the expressed reaction of system of microcirculation prevail. In process of V.'s zatikhaniye or transition of process to a subacute form the vascular phenomena calm down and into the forefront the phenomena of proliferation dominating at hron act. B. At hron, abscess, e.g., along with formation of pus there are expressed proliferative phenomena up to development of mature connecting fabric. At the same time proliferative small knots with very poorly expressed vascular and exudative reaction arise initially at nek-ry infectious diseases with an acute current (belly and sypny typhus, malaria, a tularemia).

At hron, an inflammation with a wavy current the wedge, a picture can be very motley depending on dominance of this or that phase B., and in fabrics changes are possible both old, and fresh morfol.

The main clinical signs

Five classical a wedge, the signs characteristic of acute V. of investments, keep the value, having stood the test of time and having received modern patofiziol. and morfol, characteristic: redness, swelling, pain, temperature increase, dysfunction. At hron. Century and V. of internals nek-ry of these signs can be absent.

Redness — very bright wedge, V.'s sign caused by a peristatic hyperemia, expansion of arterioles, venules, capillaries, delay of a blood flow; in process of delay of a blood flow scarlet-red coloring of the inflamed fabric becomes cyanotic. The peristatic hyperemia is combined with alteration of the fabric raised by vascular and fabric permeability, exudation and proliferation of cells i.e. with all complex of the fabric changes characteristic of Century.

Swelling at V. it is caused in an initial stage by effects of vascular reaction and the formation of infiltrate and perifocal hypostasis developing especially easily around the center of V. surrounded with friable fabric; during later periods of V. also proliferation matters.

Pain — the constant satellite B. resulting from irritation exudate of the terminations of sensory nerves or nek-ry physiologically active agents, napr, a kininama.

Temperature increase develops at the strengthened inflow of an arterial blood, and also as a result of increase in a metabolism in the center of Century.

Dysfunction because of V. arises, as a rule, always; it can sometimes be limited to disorder of functions of the struck fabric, but all organism, especially suffers more often when V. arises in vitals.

The main forms of an inflammation

On morfol, to signs distinguish three forms B.: alterativny, exudative, productive (proliferative).

The Alterativny inflammation

the Alterativny inflammation is characterized by dominance of damage of fabrics though exudation and proliferation also take place. This type of V. call also parenchymatous since it is observed most often in parenchymatous bodies (a myocardium, a liver, kidneys, skeletal muscles).

Alteration is expressed various look by dystrophy of cells of a parenchyma of body and a stroma, beginning from muddy swelling of cytoplasm and finishing necrobiotic and necrotic changes, to-rye can arise in a parenchyma of body and in interstitial fabric in the form of fibrinoid swelling and a fibrinoid necrosis.

Fig. 1. Alterativny myocarditis. In the center the site of a myocardium deprived of muscle fibers with preservation of elements of a stroma.

Alterativnoye V. with dominance of necrobiotic changes is called necrotic Century. Such type B. is observed at allergic reaction of immediate type (see the Allergy), and also at influence is strong toxics. At impact on an organism of toxins of bacteria, napr, diphtherias, there is alterativny V. of a myocardium, a cut is expressed by emergence in various layers of a myocardium, especially in a subendocardial zone, the centers of fatty dystrophy, glybchaty disintegration of myofibrils up to emergence in hard cases of the centers of a necrosis; the same is observed at allergic myocarditis (tsvetn. fig. 1). Sosudistomezenkhimalny and proliferative reactions at the same time are expressed poorly.

In a liver alterativny V. is observed at infectious hepatitis, at influence, e.g., of chloroform, perchloromethane and expressed by muddy swelling and fatty dystrophy of hepatocytes, increase in their size and size of a liver in general.

In a kidney alterativny V. is expressed by granular dystrophy of an epithelium of proximal and distal departments of nephron up to a necrosis of an epithelium at poorly expressed vascular and mesenchymal reaction.

Alterativny V.'s outcomes are defined by intensity and depth of defeat of fabric. At easy degree of dystrophy after elimination of the reason which caused V. there comes the complete recovery of fabrics; sites of irreversible damage of a parenchyma are replaced with connecting fabric (e.g., after diphtheritic myocarditis the cardiosclerosis develops).

The exudative inflammation

the Exudative inflammation is characterized by dominance of reaction of system of microcirculation, hl. obr. its venulyarny department, over processes of alteration and proliferation. Into the forefront exudation of liquid parts of plasma, emigration of blood cells, i.e. formation of exudate acts. A variety morfol, and a wedge, manifestations since depending on extent of disturbance of vascular permeability character of exudate can be a miscellaneous is typical for exudative V. In this regard exudative V. can be serous, catarral, fibrinous (croupous and diphtheritic), purulent, putrefactive, hemorrhagic, mixed.

Serous inflammation it is characterized by accumulation in fabrics, is more often in serous cavities, slightly muddy, almost transparent exudate containing from 3 to 8% of protein of serum, and in draft — single segmentoyaderny granulocytes and desquamated cells of serous covers.

Thermal (burns), chemical, infectious (especially viruses), endocrine, allergic agents can be serous V.'s cause. This form B. develops in serous cavities more often (serous pleurisy, peritonitis, a pericardis, arthritis, etc.), is more rare in parenchymatous bodies — a myocardium, a liver, kidneys.

Fig. 2. Serous pneumonia. A plethora of capillaries of alveolar partitions, in a gleam of alveoluses — serous liquid with desquamated alveolotsita (1) and with the breaking-up segmentoyaderny leukocytes.

Serous V. of a myocardium is expressed by accumulation of exudate between bunches of muscle fibers, around capillaries; in a liver — in vokrugsinusoidny spaces (Disse's spaces); in kidneys (at a serous glomerulitis) — in a gleam of the capsule of a ball (Shumlyansky's capsule — Boumena). In a lung the serous exudate accumulates in a gleam of alveoluses (tsvetn. fig. 2). At a burn of skin the serous exudate collects under epidermis that leads to formation of large bubbles. In serous covers the hyperemia is noted, they become dim, lose gloss inherent to them.

The serous exudate can arise around purulent V.'s centers (e.g., at a periostitis of a jaw) or around a tuberculous focus, increasing the area of defeat — so-called perifocal V.

Seroznoye V. usually proceeds sharply. At a large number of an exudate cordial activity is at a loss, there is a respiratory insufficiency, mobility of joints, etc. is limited.

Serous V.'s outcome if it did not pass in purulent or hemorrhagic, generally favorable. Serous exudate easily resolves and does not leave any marks or the insignificant thickening of serous covers is formed. In a myocardium and a liver there can be small sites of a sclerosis because of proliferation of fibroblasts and formation of collagenic fibers.

Catarrh (Qatar) develops on mucous membranes and it is characterized by formation of liquid, often transparent exudate with impurity of a large amount of slime, to-ruyu in the increased quantity emit mucous glands. Exudate contains leukocytes, lymphocytes and desquamated epithelial cells and usually as if flows down on a mucous membrane. Are that catarral rhinitis, rinosinusit, gastritis, a coloenteritis. On character of exudate, i.e. on dominance of these or those elements in exudate, speak about serous, mucous or purulent katar. Century of a mucous membrane quite often begins with serous Qatar, to-ry passes in mucous, then into purulent.

The reasons are very various. Microbes, thermal and chemical irritants are of great importance, etc. Katara can arise during the weakening of protective forces of an organism when saprophytic bacteria, vegetans on mucous membranes, become pathogenic.

Catarral V. can proceed sharply and chronically. At an acute current the mucous membrane looks plethoric, bulked up, is covered with liquid exudate. Acute serous and mucous Qatar proceeds two-three weeks and usually passes without leaving effects. At purulent Qatar on a mucous membrane there can be erosion, ulcers. At hron, Qatar in one cases the mucous membrane can long remain bulked up and become reinforced, on it polyps (hypertrophic Qatar) can appear different size, in other cases — the mucous membrane strongly becomes thinner (atrophic Qatar).

Fibrinous inflammation it is characterized by liquid exudate, in Krom the fibrinogen passing at contact with the damaged fabrics into fibrin in a short space of time collects owing to what exudate is condensed. Fibrous V.'s etiology is various: it can be caused by microbes (a diphtheritic stick, dysenteric microbes, a tubercular mycobacterium, etc.), viruses, poisons endogenous (e.g., at uraemia) and exogenous (e.g., corrosive sublimate) origins. Fibrinous V. on serous and mucous membranes is localized, is more rare — in the depth of body. Fibrinous V. usually happens acute, but in nek-ry cases can accept hron, the current or to flow wavy.

Fig. 3. Diphtheritic inflammation of a soft palate. The center of a necrosis of an epithelium, subepithelial fabrics impregnated with fibrin (1).
Fig. 7. Lung fever. Abundance of threads of fibrin (1) with impurity of leukocytes in gleams of alveoluses; X200.
Fig. 12. A croupous inflammation of a lung in a stage of gray hepatization.

On a surface of serous covers fibrin drops out in the form of fleecy masses, and on the surface of mucous membranes — in the form of a solid film (tsvetn. fig. 3). In a gleam of air cells fibrin drops out in the form of fibrinous traffic jams, napr, at a lung fever (tsvetn. fig. 7) owing to what tissue of a lung becomes a dense and consistence reminds a liver (tsvetn. fig. 12).

Fig. 2. Shaggy pericardium. On certain sites of a pericardium imposings of fibrin are visible (it is specified by shooters).

Serous covers take a dim form, on them the fleecy imposings of fibrin soldered to a serous cover are formed (e.g., a shaggy pericardium — fig. 2). On mucous membranes fibrinous imposings in one cases are located rykhlo, superficially, easily separate, in others — are densely soldered to the subject fabric that depends on depth of damage and on character of an epithelium of a mucous membrane. So, communication of a prismatic epithelium with the subject fabric weak and fibrin, even dropped out in the depth of a submucosal layer, forms rykhlo the sitting film (e.g., on a mucous membrane of a stomach, intestines, a trachea, bronchial tubes).

Fig. 10. Diphtheritic tonsillitis and croupous tracheitis. The surface of almonds and a mucous membrane are covered with filmy imposings.

The flat epithelium is densely connected to the subject connecting fabric, and the film of fibrin therefore is densely soldered to a mucous membrane though fibrin and drops out in a surface layer of a flat epithelium (between the cells which remained at damage) that is observed, e.g., on a mucous membrane of almonds, an oral cavity, a gullet. Due to these features fibrinous V. (tsvetn. fig. 10) is subdivided on diphtheritic (densely sitting films) and croupous (rykhlo the sitting films).

Diphtheritic Century. proceeds more hard: under densely sitting films microbes breed, allocating a large amount of toxin; films can close respiratory tracts, napr, at diphtheria of a pharynx that can cause asphyxia. At croupous V. films easily separate, intoxication is expressed more weakly, however danger of obstruction of respiratory tracts is also not excluded.

Fibrinous V. is among severe forms of V.; its forecast considerably is defined by localization of process and depth of defeat of fabric, and fibrinous V.'s outcome of serous and mucous membranes is various. On serous covers of mass of fibrin partially are exposed to enzymatic fusion, the most part — to processes of the organization, i.e. germination by young connecting fabric from cambial layers of visceral and parietal serous covers in this connection connective tissue unions (commissures) are formed, to-rye can break function of body.

On mucous membranes fibrinous films are usually torn away thanks to to an autolysis (see), developed around the center, and to demarcation Century. On site the torn-away film defect of a mucous membrane, an ulcer is formed, depth a cut is defined by depth of loss of fibrin. Healing of ulcers sometimes happens quickly, but in nek-ry cases (especially in a large intestine at dysentery) drags on on long terms. In air cells fibrinous exudate at a favorable current of a lung fever is exposed to lytic disintegration and resolves, in rare instances exudate burgeons cells of young connecting fabric, edges gradually ripens, and there are fields of a sclerosis that is designated as carnification of a lung.

Fig. 3. A pyoderma at the child.

Purulent inflammation it is characterized by the liquid exudate containing albumine and globulins, and sometimes and threads of fibrin; in draft — the neutrophils which preferential broke up (purulent little bodies). Such product of V. — muddy, with a greenish shade liquid — is called pus (see). Purulent V.'s etiology is various: it can be caused by bacteria (staphylococcus, streptococci, gonokokk, meningokokk, are more rare than a salmonella of typhus, tubercular mycobacteria, etc.), pathogenic fungi or to be aseptichny, caused by chemical substances. Purulent V. can arise in any fabric and body, serous cavities, in skin (fig. 3). Its current can be acute and chronic, in nek-ry cases very heavy.

Fig. 8. Embolic abscess of a myocardium. In the center of abscess — a bacterial embolus (1).

Morphologically purulent V. can have two forms — abscess (see) and phlegmon (see) and to be followed by a histolysis (fusion of fabric). Abscess can initially arise (his cavity is formed as a result of fusion of fabric), and also by an embolism at a septicopyemia, napr, focal purulent V. of a myocardium with formation of abscess (tsvetn. fig. 8).

Fig. 4. Phlegmonous inflammation of a gall bladder: pieces of the smooth muscle fibers (1) which are moved apart by purulent exudate.
Fig. 5. The same drug — big increase, is a lot of eosinophils (1) in exudate.

Acute diffuse purulent V. (phlegmon) has bent to extend on interfascial layers, interfabric cracks (tsvetn. fig. 4); at phlegmon of bodies went. - kish. a path in infiltrate there are a lot of eosinophils (tsvetn. fig. 5).

At hron, a form B. the suppurative focus is surrounded with the dense fibrous capsule; in exudate along with purulent little bodies there are in a small amount lymphocytes, macrophages and plasmocytes. The periods of an aggravation of V., burrowing with the expiration of pus are possible. Accumulation of purulent exudate in nek-ry cavities of an organism is designated as empyema (see).

In acute purulent V.'s outcome in opportunities there comes the otgranicheniye of process, healing even of big abscesses by substitution of their cavity the granulyatsionny fabric which is gradually ripening in a hem is possible to-ry and remains on site abscess. Hron, purulent V. can proceed very long and bring to to an amyloidosis (see). In adverse cases the suppurative focus is not delimited, purulent process passes on limf, vessels and veins that leads to generalization of process, sometimes up to sepsis (see).

Putrefactive inflammation (gangrenous, ichorous) develops owing to participation at this or that type of exudative V. of putrefactive bacteria (pathogenic anaerobe bacterias). Putrefactive V. constitutes big danger to an organism and can arise in those bodies, to-rye adjoin to the environment (see. Gangrene , Ludwig quinsy ). The inflamed fabrics are exposed to putrefactive decomposition, get dirty-green coloring, become flabby, as if creep away with formation badly of the smelling gases (see. Mephitic gangrene ).

Hemorrhagic inflammation it is characterized by existence in exudate of different quantity of erythrocytes. Hemorrhagic character can take any kind of V. (serous, fibrinous, purulent) that depends on high extent of increase in permeability, up to destruction of vessels of microcirculation. This type of V. arises at influence of highly virulent microbes; at plague, a malignant anthrax, toxic flu the hemorrhagic center of V. reminds hemorrhage. Hemorrhagic exudate is observed in serous cavities at malignant tumors. This type of V. is a symptom of very serious illness; its outcome depends on the main disease.

The mixed forms of an inflammation are observed during the weakening of protective forces of an organism, accession of consecutive infection, e.g. stafilokokk. In these cases can join serous exudate purulent or fibrinous, then V. call serous and purulent, serofibrinous etc. The mixed character can have and catarral V. Osobenno an adverse predictive sign is transformation of serous exudate in hemorrhagic that always indicates accession of a heavy infection or progressing of a malignant tumor.

The productive inflammation

This form is called also proliferative inflammation since it is characterized by dominance of reproduction (proliferation) of cellular elements of the struck fabric. Alteration and exudation are expressed poorly, are distinguished hardly; segmentoyaderny granulocytes are single.

Productive V. can be caused initially biol., physical. and by chemical factors or it is observed upon acute V.'s transition to chronic.

Productive V. proceeds, as a rule, chronically, but there can be acute, napr, granulematozny V. at belly and a sapropyra, at vasculites of various etiology etc.

Reproduction of young cells of local connecting fabric, and also cambial cells of the circulatory capillaries, at a differentiation forming new capillaries is the cornerstone of productive V. Breeding at productive V. All cells have as a local, gistiogenny, and hematogenous origin. E.g., in V.'s center it is possible to see big and small lymphocytes, monocytes, and also in a small amount the eosinophils and basophiles which got from a blood flow. In process of maturing of cells in V.'s center there are macrophages, fibroblasts, fibrocytes, lymphoid, single plasmatic and mast cells. Productive V. is completed as if by fibroblasts; they cosecrete tropocollagen — the predecessor of collagen of fibrous connecting fabric, edges remains on site focus of productive Century.

Outcomes of a productive inflammation different. There can come the full rassasyvaniye of cellular infiltrate; however is more often on site than infiltrate as a result of maturing of the mesenchymal cells entering infiltrate connective tissue fibers are formed and there are scars.

There are two kinds of productive V.: nonspecific and specific. At nonspecific productive V. proliferating cells are located in the inflamed fabric diffuzno; morfol, the specific picture characteristic of the activator which caused V., no. At specific productive V. the cellular composition of exudate, group of cells and a cycle of process are characteristic of the activator B. Specific V. mostly has character of so-called infectious granulomas — the small knots consisting of elements of granulyatsionny fabric.

Allocate the following forms of productive V.: interstitial V., formation of granulomas, V. with formation of polyps and sharp-pointed condylomas, V. around zooparasites and foreign bodys.

Fig. 9. Acute intersticial myocarditis. Focal perivascular (around a plethoric vessel) and diffusion (1), between muscle fibers kruglokletochny infiltrates.

Interstitial inflammation, or intersticial, usually has hron, the current also is characterized by the fact that inflammatory infiltrate is formed in the stroma of body surrounding vessels (a myocardium, a liver, kidneys, lungs, cross-striped muscles, a uterus, closed glands). The infiltrate consisting of various cells is located diffuzno, occupying all body, or the separate centers preferential around vessels (tsvetn. fig. 9). In some cases any type of cells prevails; sometimes infiltrate consists of lymphocytes and macrophages and reminds V. on an immune basis. At nek-ry types of interstitial V. the large number of the plasmocytes cosecreting gamma-globulins collects. At death of plasmocytes products of their life activity remain in fabrics in the form of freely lying fuchsinophil spherical educations — so-called hyaline spheres, or russelevsky little bodies. In interstitial productive V.'s outcome develops sclerosis (see) or cirrhosis (see).

Formation of granulomas (small knots) results from reproduction of cells in interstitial fabric of body under the influence of a pathogenic factor. These small knots can consist of various mesenchymal cells or of one type of cells; sometimes they are located in close connection with small vessels and even form in a wall of an artery. Diameter of a granuloma usually does not exceed 1 — 2 mm, but can reach 2 cm. The center of a granuloma sometimes finds cellular or fabric a detritis, in Krom sometimes it is possible to reveal a disease-producing factor, and on the periphery of a detritis in different ratios macrophages lymphoid, epithelial, plasmatic and mast cells are located, among to-rykh it is possible to find multinucleate colossal cells. Usually granulomas are poor in capillaries.

Formation reflects protective and immune processes in fabrics of granulomas, to-rye develop at infectious diseases, and to a certain extent defines dynamics immunol, process from the beginning of damage of fabric to a final stage of the disease which is expressed scarring of granulomas.

Formation of granulomas is observed at a number of acute infectious diseases (belly and sypny typhus, a tularemia, viral encephalitis, rage) and nek-ry hron, diseases (rheumatism, a brucellosis, mycoses, a sarcoidosis, tuberculosis, syphilis, etc.).

At nek-ry hron, infectious diseases of a granuloma get to a certain extent characteristic of this disease morfol, a structure and dynamics of development. In this regard they are designated as follows: a hillock — at tuberculosis, a gumma — at syphilis, a leproma — at a leprosy, small knots — at a sapa and a rhinoscleroma. At the listed V.'s diseases proceeds it is specific, i.e. it is peculiar only to this disease; in specific V.'s granulomas the cellular structure is quite similar, epithelial and multinucleate colossal cells are most characteristic: Pirogov's cells — Langkhansa — in a tubercular granuloma; cells, or spheres, Virkhova — in leprose; Mikulich's cells — at a scleroma, etc.

Fig. 6. Microscopic picture of a tubercular granuloma: in the center — two huge multinucleate cells with chains of kernels on perimeter, in a circle — epithelial cells; X200.
Fig. 11. Miliary tubercular granulomas of a lung.

Specificity of granulomas is defined not only them morfol, a structure (tsvetn. fig. 6), but also features wedge. current and pathoanatomical manifestations of V. (tsvetn. fig. 11). In nek-ry cases of a granuloma at tuberculosis, syphilis and leprosy have so much the general in a structure that without special coloring of the activator the diagnosis can be complicated; therefore at morfol, specific V.'s diagnosis the kliniko-anatomic analysis of a disease in general is very important.

At a typhoid of a granuloma are formed in group limf, follicles (peyerovy plaques), in ileocecal limf, nodes, a liver, a spleen, marrow. They arise from the proliferating reticular macrophages capable to englobe typhus salmonellas; these nodular accumulations then are exposed to a necrosis. Process of formation of a granuloma, including formation of a hem, takes 4 — 5 weeks (see. Typhoid ).

Granulomas at a sapropyra arise in c. the N of page, especially in a myelencephalon at the level of olives, in close connection with small vessels, in to-rykh is observed a productive and destructive endothrombovasculitis, characteristic of a sapropyra (see. Sapropyra epidemic ). Granulomas, similar on a structure, but with less expressed defeat of vessels arise in c. N of page at viral encephalitis and rage.

At rheumatism of a granuloma arise in connecting tissue of a myocardium, valves of heart, in circumarticular fabric, in the capsule of almonds; they are constructed of cells, large with basphilic cytoplasm of macrophagic type, accumulation to-rykh is considered as reaction to processes of disorganization of connecting fabric (see. Rheumatism ).

At a tularemia the granuloma develops in regional to the center of damage of skin limf, nodes. In the center of a granuloma — the center of a necrosis, on the periphery — a shaft from epithelial and lymphoid cells and a large number of segmentoyaderny granulocytes; sometimes multi-core colossal cells meet (see. Tularemia ).

At a brucellosis of a granuloma have a different structure. In one cases in the center of a granuloma and for a circle accumulation of epithelial and huge multinucleate cells, in others — in the center of a granuloma a necrosis and on the periphery epithelial and colossal cells is observed (see. Brucellosis ); morfol, the picture is very similar to a tubercular granuloma.

The sarcoidosis is characterized by formation in limf, nodes of the granulomas constructed of epithelial and colossal cells without signs of a necrosis in the center (see. Sarcoidosis ).

During the healing of granulomas small, scarcely noticeable scars are formed (see. Granuloma ).

Formation of polyps and sharp-pointed condylomas — productive V. of mucous membranes. At the same time expand a stromal cell and a prismatic epithelium, polyps of an inflammatory origin (hypertrophic Qatar) are formed; polypostural rhinitis, colitis, etc. are that, e.g. On mucous membranes, on border of a prismatic and flat epithelium, napr, in an anus, on generative organs, sharp-pointed condylomas are formed of growths of a flat epithelium (see Warts). The discharge of mucous membranes irritates and macerates a flat epithelium, in a stroma causes hron. Century, a cut stimulates a stroma and an epithelium to further growth (see. Papilloma , Polyp , polyposes).

At implementation in fabric of zooparasites, foreign bodys there is also productive V. as reactive process of an organism. Foreign bodys (e.g., a splinter of a shell) are surrounded granulyatsionny fabric (see), usually with impurity of the multinucleate colossal cells which are taking part in a rassasyvaniye of foreign bodys; around the remains of a foreign body the fibrous capsule forms. The died zooparasites, napr, trichinellas, a cysticercus, become impregnated with salts of lime (petrification).

The inflammation and reactivity of an organism

the Favorable current of V. is defined by perfection of processes of phagocytosis, antibody formation, proliferation of connective tissue cells, an otgranicheniye of the inflammatory center. Such proper response is inherent to a healthy organism and is called normergicheskoy. However development of all components B., a current and an outcome depend also on a condition of an organism: from the previous diseases, age, metabolic rate, etc.

Klin, observations show that often same activator in one person does not cause any reaction, and in another — very rough local and general reaction leading sometimes even to death.

Cases of diphtheria when in a family one person perished from heavy toxic display of a disease are described, e.g., and other family members or did not get sick at all, or their infection was shown in the erased form of a disease though all had one source of infection.

It is established what depending on reactivity of an organism of V. can be giperergichesky, arising in a sensibilized organism (see. Allergy ), or gipoergichesky, a cut

many observations when the picture B. does not correspond to usual, normergichesky type are observed with immunity to the agent V. Imeetsya and depend not so much on toxicity of the activator how many from inadequately rough reaction of the struck organism that can be caused preliminary sensitization (see). This type B. is called allergic m an inflammation.

In an experiment at the animals infected with a diphtheritic stick after a sensitization horse serum, the disease proceeds very violently and peculiar in comparison with not primed animals. The fact that such disease, other than normergichesky, is connected with a sensitization of an organism, was noted even in works on G. P. Sakharov (1905) anaphylaxis, on tuberkulinovy reaction To. A tuberculine test (1907), in researches about morphology of allergic reactions of A. I. Apricot (1938) and Ruble Ressle (1935), in works about V.'s development in ontogenesis of H. N. Sirotinin (1940).

An inflammation on an immune basis

Researches F. Burnett (1962), R. V. Petrov (1968) are established that V.'s rates can amplify or be slowed down depending on a condition of cellular and humoral immunity, i.e. at the changed reactivity of an organism of V. gains the features distinguishing it from normergichesky V. Tak, introduction to an organism as antigen of a proteic matter leads to development of hypersensitivity and at repeated introduction even of an insignificant dose of the same substance inadequate general or local reaction with accurately expressed difference from normergichesky reaction — discrepancy between a small dose of antigen and very rough reaction of an organism develops (see. Anaphylaxis , Artyusa phenomenon ).

Such reaction is called giperergichesky, V. — giperergichesky, or hypersensitivity reaction of immediate type: it develops in fabrics in 1 — 2 hour after repeated administration of antigen. Cell-bound immune complexes are V.'s reason at immediate hypersensitivity, to-rye consist of the antibody circulating in blood on the antigen entered earlier, the antigen which is again entered into fabric and the activated complement. Kokrin (Ch. Cochrane, 1963) showed that cell-bound immune complexes possess cytopathic and leykotaksichesky effect: they are fixed in a vascular wall, especially post-capillary venules, damage it, increasing permeability and a leukodiapedesis.

At the allergic V. proceeding as reaction of immediate hypersensitivity from fabrics the so-called inflammatory protease (rich with sulphhydryl groups) which is sharply increasing vascular permeability and stimulating emigration of segmentoyaderny granulocytes is released. At this type B. both in an experiment, and in pathology the person has a considerable damage of fabrics, very expressed reaction of a microcirculator bed, plentiful emigration of segmentoyaderny granulocytes, plasmatic treatment and a fibrinoid necrosis of walls of small vessels and the fabrics surrounding vessels, hypostasis, hemorrhages, i.e. the characteristic picture of necrotic Century develops. The immune nature of this V. is confirmed by detection in the center of the cell-bound immune complexes determined by Koons's method (see. Immunofluorescence ).

Elektronnomikroskopichesky and immunochemical researches of Shirasava (H. Schirasawa, 1965) show the following sequence of fabric changes in isherergichesky V.'s center of immediate type: 1) formation of immune precipitated calcium superphosphates (complexes antigen — an antibody) in a gleam of venules; 2) linkng with a complement; 3) hemotaksichesky effect of precipitated calcium superphosphates on segmentoyaderny granulocytes and their accumulation about veins and capillaries; 4) phagocytosis and digestion of cell-bound immune complexes segmentoyaderny granulocytes by means of enzymes of lysosomes; 5) release of lysosomic enzymes and formation of vasoactive substances; 6) damage of a vascular wall by them with the subsequent hemorrhage, hypostasis and a necrosis.

Giperergichesky inflammation, i.e. Century, proceeding on an immune basis, it is observed at the patients inclined to allergic reactions, naira, at medicinal intolerance, in an acute phase of a course of collagenic diseases, at hay fever, etc.

There is also other type of hypersensitivity of an organism — hypersensitivity of the slowed-down type; manifestations not of humoral, but cellular immunity are the cornerstone of it. At the same time local reaction in fabrics of a sensibilized organism arises in 12 and more hours after repeated administration of the corresponding antigen. Such reaction is usually observed at the children infected with a tubercular mycobacterium after intradermal administration of tuberculine therefore reaction of hypersensitivity of the slowed-down type is called also reaction of tuberkulinovy type. The main role in such V.'s center belongs to T lymphocytes and macrophages. Lymphocytes are representatives of population of thymic lymphocytes, they migrate from lymphoid bodies in blood and back (recirculating lymphocytes), as if find antigen in fabrics and carry out pathogenic action on fabric. Lymphocytes come into contact with macrophages rich with acid phosphatase and as if mutually inform each other on the nature of antigen. Changes of a microcirculator bed in V.'s center at this type of reaction are expressed very poorly, segmentoyaderny granulocytes are absent, V.'s signs are expressed vaguely. Between subjects B., proceeding as the slowed-down hypersensitivity, it is observed at a number of serious autoimmune illnesses (in skin, a liver, kidneys, etc.). having poorly expressed a wedge, and morfol, to the loudspeaker, also comes to an end with a sclerosis.

Quite often gistol, the picture at hron, interstitial V. at the person reminds reaction of the slowed-down type (dominance in infiltrate of lymphocytes and macrophages); Accepts a long current century, reflecting the autoimmune processes proceeding in an organism. The same type B. is observed during the formation of granulomas. In one cases of a granuloma perform function of macrophages concerning antigen, in others — the granuloma is as if intended for a resorption of decomposition products of fabrics in the center of immune destruction (e.g., a rheumatic granuloma).

Century, developing on an immune basis, it can be shown in the mixed form when it is difficult to establish borders between two kinds of giperergichesky V.

Differentiation of an inflammation and morphologically similar processes

does not present great difficulties for a wedge In the developed V.'s form, and morfol, diagnoses. However only morfol, it is impossible to be limited to criterion at V.'s recognition, its especially separate forms; it is necessary to consider all complex of manifestations, including a wedge, data. In an organism such fabric and vascular and cellular reactions as, e.g., at hypersensitivity of the slowed-down type when it is difficult to find all signs of V. in fabrics are observed: e.g., there is no expressed reaction of vessels of microcirculation, there are no segmentoyaderny granulocytes or as it is observed in a wall of a stomach in the heat of digestion, it is a lot of segmentoyaderny granulocytes as manifestation of a distribution leukocytosis. It is known that at puerperal involution of a uterus in ferruterous bodies it is possible to find infiltrates from lymphoid cells as expression of metabolic shifts. The expressed proliferation of plasmablasts and plasmocytes which does not have relations to V. in bodies of an immunogenesis (marrow, limf, nodes, a spleen, a thymus) as expression of defense reaction, is described by the shown development of antibodies. In near lokhanochny cellulose the centers of an extra marrowy hemopoiesis reminding inflammatory infiltrate are described.

Great difficulties arise at differentiation of inflammatory and dystrophic processes, inflammatory proliferation of cells and proliferation of cells of noninflammatory character, in particular tumoral.

Outcomes and value of an inflammation for an organism

V.'s Outcomes are various and conditions of an organism and structure of body depend on the reason. Death of the vital fabrics with the most serious consequences for an organism is possible. However usually inflamed fabric is gradually delimited from surrounding healthy fabric, products of fabric disintegration are exposed to zymolysis and rezorbirutsya by phagocytosis, are soaked up by capillaries neogenic limf. networks. Thanks to cellular proliferation V.'s center is gradually replaced granulyatsionny fabric (see). If considerable damage of fabrics was not, there can come their complete recovery. At a major defect on site of V.'s center as a result of maturing of granulyatsionny fabric it is formed hem (see). In bodies and fabrics there can be these or those patol, the changes (a thickening and commissures of serous covers, overgrowing of serous cavities, hems in bodies) breaking in hard cases function of region body, sometimes — all organism. So, e.g., the fibrinous exudate on a surface of serous covers, in a gleam of alveoluses can resolve or, at its considerable accumulation, is exposed to the organization and connective tissue transformation. Diffusion interstitial productive V. usually comes to an end with a diffusion sclerosis of body (e.g., a cardiosclerosis). During the healing of a large number of granulomas, napr, in a myocardium at rheumatism, the considerable fields of a cardiosclerosis which are negatively affecting action of the heart are formed. When the arisen connecting fabric shrivels and squeezes a parenchyma, the body is deformed that usually is followed by reorganization of its structure and the phenomena regenerations (see). Such process is designated as cirrhosis of body, napr, cirrhosis, nefrotsirroz, pneumocirrhosis.

An inflammation — important zashchitnoprisposobitelny and in the all-biological plan rather reasonable reaction developed in the course of phylogenesis; this reaction gradually became complicated in the course of evolution of live organisms (see. Defense reactions of an organism , Adaptive reactions ). Bears protection against influence of a pathogenic factor in the form of a peculiar biol, a barrier century that is expressed by the phenomenon of phagocytosis and development of cellular and humoral immunity. However it is reaction automatic, it is carried out on mechanisms of self-control by means of reflex and humoral influences. Arising as adaptive reaction, V. under certain conditions can gain sometimes harmful value for an organism: at V. there is a damage of fabrics, at nek-ry forms up to a necrosis.

Thanks to inflammatory reaction there is an otgranicheniye of focus of damage from all organism, emigration of white blood cells to V.'s center and phagocytosis, elimination of the harmful beginnings. Proliferation of lymphocytes and plasmocytes promotes development of antibodies and increase in local and general immunity. At the same time it is well known that accumulation of exudate at V. can be very dangerous. So, e.g., exudate in alveoluses at pneumonia already from the very beginning of the emergence exerts an adverse effect on an organism since gas exchange is broken, education on a mucous membrane of a throat of a fibrinous exudate causes narrowing of a gleam, irritates receptors of a throat that is followed by a spasm of muscles of a throat and can bring to asphyxia (see). Phagocytosis can be incomplete: the phagocyte which absorbed a bacterium, but not capable to digest it, becomes a carrier of an infection on an organism.

Disturbances at V. not only local; usually there is also the general reaction of an organism, expressed fever, a leukocytosis accelerated ROE, change of protein and carbohydrate metabolism, the phenomena of the general intoxication of an organism that in turn changes reactivity of an organism.

I. I. Mechnikov in 1892 wrote: «... the salutary force of nature which main element is made by inflammatory reactions is not still adaptation which reached perfection at all. Private diseases and cases of premature death prove it enough». And further: «This imperfection made necessary active intervention of the person unsatisfied with function of the natural salutary force». Imperfection of «the salutary force» of the nature does necessary surgical intervention and use of the therapeutic funds allocated for strengthening of defense and compensatory reactions of an organism and

V. V. elimination is the cornerstone of many diseases therefore also the wedge, medicine is one of the major problems experimental. It is studied at all levels biol, structures, starting with molecular, subcellular, cellular and finishing a complete organism. Are investigated etiol, factors, biochemical, changes, morfofiziol. characteristics, reactivity of fabrics and organism in general, wedge, picture B. There was a special section in development of a problem B. — V.'s pharmacology — studying of mechanisms of action of mediators of V., with participation to-rykh various stages of inflammatory reaction are implemented; the active antiinflammatory drugs which are slowing down allocation of these mediators, therefore promoting a zatikhaniye of Century are found.

Bibliography: Ado A. D. Pathophysiology of phagocytes, M., 1961, bibliogr.; Alekseev O. V. and Chernukh A. M. Ney-ro-kapillyarnye bonds in a myocardium of rats, Bulletin Ekspery, biol, and medical, t. 74, No. 12, page 96, 1972, bibliogr.; Alpern D. E. Inflammation (Questions of a pathogeny), M., 1959, bibliogr.; Voronin V. V. Inflammation, Tbilisi, 1959, bibliogr.; An inflammation, immunity and hypersensitivity, the lane with English, under the editorship of G. 3. Moveta, M., 1975; Kongeim I. The general pathology, the lane with it., t. 1, SPb., 1887; The M e Tax Code of ying V. Dinamik of an inflammation, the lane with English, M., 1948, bibliogr.; Swordsmen I. I. Ocherk of the current state of a question of an inflammation, SPb., 1897; it, Lectures about comparative pathology of an inflammation, M., 1947; Paskhina T. S. A role of humoral factors of the peptide and proteinaceous nature in regulation of capillary permeability, Vestn. USSR Academy of Medical Sciences, No. 9, page 21, 1962; Pigarevsky V. E. Cytochemistry of antibacterial cationic proteins of leukocytes at phagocytosis and an inflammation, Arkh. patol., t. 37, No. 9, page 3, 1975, bibliogr.; G1 about l and carat And. Inflammatory reactions and their dynamics, the lane with fr., Novosibirsk, 1969, bibliogr.; Strukov A. I. Controversial issues in the doctrine of an inflammation, Arkh. patol., t. 34, No. 10, page 73, 1972, bibliogr.; Chernukh A. M. Infectious center of an inflammation, M., 1965, bibliogr.; Chernukh A. M., Alexandrov P. N. and Alekseev O. V. M! ikrotsirkulya-tion, M., 1975, bibliogr.; With about t r a n R. S. The fine structure of the microvasculature in relation to normal and altered permeability, in book: Physical bases of circulatory transport, ed. by E. B. Reeve a. A. C. Guyton, p. 249, Philadelphia — L., 1967, bibliogr.; H i r s with h J. G. Phagocytosis, Ann. Rev. Microbiol., v. 19, p. 339, 1965, bibliogr.; The inflammatory process, ed. by B. W. Zweifach a. o., v. 1 — 3, N. Y. — - L., 1974; Mediators of inflammation, ed. by G. Weissmann, N. Y., 1974; M i 1 e s A. A. Large molecular substances as mediators of the inflammatory reaction, Ann. N. Y. Acad. Sci., v. 116, p. 855, 1964; M i 1 es A. A. a. Wilhelm D. L. Globulins affecting capillary permeability, in book: Polypeptides which effect smooth muscles a. blood vessels, ed. by M. Schach-ter, p. 309, Oxford a. o., 1960, bibliogr.; Rocha e Silva M. Chemical mediators of the acute inflammatory reaction, Ann. N. Y. Acad. Sci., v. 116, p. 899, 1964; Selye H. The mast cells, Washington, 1965, bibliogr.; Spector W. G. Activation of a globulin system controlling capillary permeability in inflammation, J. Path. Bact., v. 74, p. 67, 1957, bibliogr.; it, Substances which affect capillary permeability, Pharmacol. Rev., v. 10, p. 475, 1958, bibliogr.; Spector W. G. a. Willoughby D. A. The inflammatory responce, Bact. Rev., v. 27, p. 117,1963; they, The pharmacology of inflammation, L., 1968; Willoughby D. A. a. Walters M. N. The effect of ribonucleic acid (RNA) of on vascular permeability and its possible relation to LNPF, J. Path. Bact., v. 90, p. 193, 1965.

A. I. Strukov, A. M. Chernukh.