THROMBOSIS (thrombosis; Greek throm-bos a piece, a clot + - osis) — an intravital blood coagulation in a gleam of a vessel.
Development of thrombosis conducts to a circulatory disturbance in fabrics (see the Heart attack, the Stroke) and complicates the course of diseases. In a healthy organism of a condition for formation of blood clot are absent owing to the functional interaction coordinated by nervous and endocrine systems between the factors leading to aggregation of thrombocytes and a blood coagulation and the factors interfering it and also between coagulant and fibrinolitic systems of blood.
At the heart of a pathogeny of T. damages of walls of vessels, changes of a functional condition of system of a hemostasis (see) and delay of a blood-groove lie. According to E. I. Chazov and D. M. Zubairov, the prime cause of T. damage of a vascular wall is, against the background of to-rogo occur adhesion (see t. 20, additional materials) and aggregation of thrombocytes (see) with formation of primary thrombocyte of rny blood clot, and also activation of synthesis of prostaglandins (see) in thrombocytes, coagulant system of blood, local hypercoagulation, release of a factor of the XIII coagulant system of blood and local braking of a fibrinolysis (see).
Damage of walls of vessels can be structural as a result of an injury, infections, reaction antigen — an antibody, etc. also functional (decrease in anti-thrombogenic activity of a vascular wall owing to disturbance of synthesis of prostacyclin — the most powerful endogenous inhibitor of aggregation of thrombocytes and a plasminogen activator, napr, at a stress, atherosclerosis, burns idr.). The factors causing functional. damage of a vascular wall, according to V. P. Baluda, K. M. Lakin (see t. 15, additional materials), etc., are the adrenaline, noradrenaline and cortisol allocated in considerable quantities at an emotional stress (see), so-called neotreagirovanny emotions and also activation of peroxide oxidation of lipids, napr, at impact of ionizing radiation, burns, atherosclerosis. In a pathogeny of T. the combination of structural and functional damages of a vascular wall matters. At structural damages local conditions for aggregation of thrombocytes, activation of a factor of the XII coagulant system of blood are created. However with a high speed of a blood-groove and anti-thrombogenic activity of a vascular wall, at a cut in blood prostacyclin, conditions for emergence of T is constantly emitted. no. At functional damage the action of a vascular wall inhibiting trombogenez is eliminated, conditions for acceleration of a blood coagulation, spontaneous aggregation of thrombocytes and
T. T. development are created arises more often at disturbance biol. reliability of system of a hemostasis that is observed at the damage of its regulatory mechanisms conducting to a prethrombotic state (thrombophilia). The thrombophilia arises owing to change of one or several components of system of a hemostasis — thrombocytes (a thrombocytosis, increase in functional activity of thrombocytes — adhesion, aggregation, reaction of release), blood-coagulation factors (see. Coagulant system of blood), factors of a fibrinolysis (decrease in content of plasminogen and its activators, increase in activity of inhibitors of plasminogen activators and plasmin), factors of a vascular wall (decrease in synthesis of prostacyclin, anti-aggregation, antitrombino-gene properties of an endothelium, activity of plasminogen activators).
In a pathogeny of T. disturbances of a blood-groove and a vasospasm matter. So, more frequent formation of blood clots in veins, than in arteries, is connected with slower blood-groove in them. However delay of a blood-groove is not the prime cause of a thrombogenesis. At dead stop of a blood-groove in a vessel, bandaging to-rogo in experimental conditions is performed without damage of an internal cover, blood in its gleam does not turn for a long time.
Along with delay of speed of a blood-groove in a thrombogenesis the nature of the movement of blood — its turbulent flow in sites with patholologically the changed wall matters (a varicosity, aneurisms, atherosclerotic plaques, a stenosis of a gleam, twisting vessels, etc.). At the same time food of an endothelium of vessels is broken, conditions for sedimentation and sticking to a vascular wall of thrombocytes, delays of thrombin and the fibrin which are formed at activation of coagulant system of blood are created.
An essential role in a pathogeny of T. play also such factors as obesity, injuries, advanced age, oncological, allergic, cardiovascular diseases, etc. Development of T. at patients of advanced and senile age it is connected with age frustration of a hemodynamics, disturbances in system of a hemostasis, structural changes of vascular walls, and also with age changes of function of the vital systems and bodies (see the Old age, aging).
Distinguish several stages of a thrombogenesis (trombogenez):
The I stage — the damage of a vascular wall leading to local activation of system of a hemostasis; The II stage — adhesion of thrombocytes to the damaged site of a vascular wall; The III stage — accumulation and aggregation of thrombocytes at the place of damage of a vascular wall; The IV stage — formation of the thrombin turning fibrinogen into fibrin in threads to-rogo thrombocytes, leukocytes and erythrocytes are late that leads to formation of blood clot; The V stage — retraction of blood clot (see Retraction).
It is possible T. main vessels (arterial and venous) and T. microcirculator bed. At arterial T. the most important factor of a trombogenez is damage of a vascular wall, at venous special value have hypercoagulation and staz blood. In genesis of T. vessels a microcirculator-nogo of a bed decisive factors are change of composition of blood, its intravascular coagulation, release of ATP from thrombocytes and erythrocytes, delay of a blood flow.
Ilo to the relation to a gleam of a vessel distinguish pristenochny blood clots (tsvetn. the tab., Art. 304, fig. 1,6) and occlusive (closing all gleam of a vessel). On a structure allocate the white, red, mixed (layered) and hyaline blood clots. White (agglyutinatsionny, or a game-glyutinatsionny) blood clot consists generally of fibrin (see), the agglutinated N of the aggregated thrombocytes and leukocytes. Macroscopically it has white or gray coloring, is located usually pristenochno (tsvetn. tab., Art. 304, fig. 2). White blood clot slowly in the conditions of rather bystry blood flow in arteries is formed; it is localized, as a rule, between trabecular muscles of an inner surface of heart, on shutters of valves of heart (tsvetn. the tab., Art. 304, fig. 5) at an endocarditis (see).
Red (coagulative) blood clot is formed at a bystry blood coagulation in the conditions of delay of a blood-groove, usually is occlusive and is more often localized in veins (tsvetn. tab., Art. 304, fig. 3). Macroscopically fresh blood clot of red color, gets further brownish coloring, becomes friable with slightly corrugated surface. Microscopically red blood clot along with fibrin, thrombocytes and leukocytes contains a significant amount of the erythrocytes defining its coloring.
The mixed (layered) blood clot consists of elements of white and red blood clots; it is localized in veins, arteries, in aneurisms of arteries and hearts. Macroscopically in it distinguish a head, as a rule, having structure of white blood clot, the neck or a middle part consisting of elements of white and red blood clots and the tail having a structure of red blood clot. The head of blood clot according to the place of its primary emergence has the conic or flattened form, is soldered to a vascular wall; in a vein it is turned by the basis towards heart, and into arteries — from heart. The tail of blood clot is located in the direction of a blood flow; it rykhlo is attached to a neck therefore can come off and be a source of a thromboembolism (see).
Hyaline (capillary) blood clots usually are located in vessels of a microcirculator bed and are found only at microscopic examination. They consist of compact fibrin and precipitated calcium superphosphates of proteins of a blood plasma or thrombocytes with impurity of fibrin.
According to Nordstagi (To. Nordsta-ga), they consist hl. obr. from the died erythrocytes with impurity of fibrin and single leukocytes.
Distinguish the localized and progressing blood clots. The localized blood clots are located preferential in arteries and occupy the limited site, napr, on an atherosclerotic plaque. The progressing blood clots meet preferential in venous system. They are limited either any to one, or several areas.
Special types of blood clots are marantic, tumoral, septic blood clots. Marantic blood clot arises at exhaustion, in the conditions of dehydration of an organism (see) and pachemias. It is formed usually in superficial veins of extremities and in sine of a firm meninx. Macroscopically marantic blood clot usually is mixed. Tumoral blood clot arises during the growing of fabric of a tumor into vessels. At the same time on the surface of intravascular tumoral growths the mixed blood clots are formed. Septic blood clot (white or mixed with presence of bacteria) is formed usually in veins at inflammatory process in a wall of a vein and the fabric surrounding it. Septic blood clot results from also primary damages of an endothelium by the bacteria circulating in blood or secondary hit of bacteria from blood in earlier formed blood clot. The blood clots which are formed in veins at their catheterization can be exposed to secondary infection (see. Resuscitation pathology).
The special form is represented by spherical blood clot in the left auricle at a mitral stenosis (see the Heart diseases acquired). There is it from the come-off pristenochny blood clot of an auricle or an ear of heart. Spherical shape to blood clot is given by power sanding of new trombotichesky stratifications and the constant movement of blood clot in a cavity of an auricle. Blood clots in auricles sometimes are exposed to mucous dystrophy (see) that gives them looking alike a myxoma (see).
On process of blood clot in it there can be a putreform aseptic softening under the influence of proteolytic enzymes of trombotichesky masses and proteases of polymorphonuclear leukocytes. Mezhtrabekulyar-ny blood clots of a left ventricle of heart are exposed to the most often putreform softening. Macroscopically at the same time in the center of blood clot kashitseobrazny weight is found liquid, sometimes. In white blood clot she has white-yellow coloring and reminds pus, in red blood clot — krasnokorichnevy. If the softening reaches a surface of blood clot, then this weight comes to a blood stream and can be a source of embolisms (see).
THROMBOSIS of VESSELS of the BRAIN 301
Organization of blood clot consists in changes of the blood clot and a vascular wall (tsvetn. tab., Art. 304, fig. 4). Cellular elements of blood clot gradually break up and merge in homogeneous mass, threads of fibrin and thrombocytes turn into gia-linopodobny masses. In trombotichesky masses fatty inclusions and glybk of hemosiderin can be found. In cells of an endothelium, adjacent to blood clot, during the first 10 days swelling, proliferation and growing into thickness of blood clot cellular tyazhy, creating capillaries is noted. Besides, cells of an endothelium proliferate and creep on a surface of blood clot. This so-called endotelization of blood clot begins in 48 hours after its education and comes to an end in several days. It is experimentally shown that in 3 — 5 days after developing of blood clot in it mesenchymal cells of a different origin appear: mononuklear-ny macrophages, the smooth muscle cells proliferating from a muscular coat of a vessel and also the fibroblasts which are together with smooth muscle cells producers of collagen, gliko-zaminoglikan, elements of a basal membrane. In the outcome of the organization of pristenochny blood clot in an internal cover of a vessel the fibromuscular plaque, sometimes with intracellular inclusions of lipids forms. According to Wolf (N. Woolf), such plaques in experimental conditions are formed in 6 months after developing of blood clot. At the organization of the blood clots occupying more than a half of a gleam of a vessel or all its gleam, again formed capillaries join in the general blood stream, i.e. there comes the sewerage of blood clot. Again formed capillaries sometimes create the large vascular cavities (so-called cavernous transformation of blood clot) improving a blood stream in the thrombosed vessel.
In blood clots with the unfinished phenomena of the organization there are centers of a gialipoz (see), sites of petrification (see Petrifikat) and the ossifications (see Ossificates) which are easily revealed with the help rentgenol. researches. Usually such petri-fitsirovanny blood clots meet in veins and carry the name of creams of tartar (phleboliths).
Heavy complication of T. the thromboembolism (see) — a separation of blood clot or its parts and their free movement in a blood-groove is. More often the thromboembolism is observed in venous system at T. veins of the lower extremities. Special danger is constituted by a thromboembolism of pulmonary arteries (see).
See also Thrombosis of vessels of a brain, Thrombophlebitis, Obliterating defeats of vessels of extremities.
Bibliography: Urgent problems haemo-staziologii, under the editorship of B. V. Petrovsky, etc., M., 1981; B and l at d and Accusative, JI of joint stock company and K. M. N and D e I am a N about in I. Trombo-filiya and trombofilichesky vigilance, Klin, medical, t. 59, No. 5,
page 11, 1981; The Inflammation, immunity and hypersensitivity, under the editorship of G. 3. Moveta, the lane with English, M., 1975; Gavri
O. K's fishing. Biological patterns of system of regulation of aggregate state of blood and problem of its studying, Probl. gematol. and modulation. blood, t. 24, No. 7, page 3, 1979; Davydovsky I. V. General pathology, M., 1969; 3 at and and r about in D. M. Biokhimiya
of a blood coagulation, M., 1978; Kudryashov B. A. Biological problems of regulation of liquid state of blood and its coagulation, M., 1975; To at z N and to B. I. About a role of a vascular wall in the course of a hemostasis, Usp. sovr. biol., t. 75, century 1, page 61, 1973; Mogosh G. Fibrinferments and embolisms at cardiovascular diseases, the lane from Romanians., Bucharest, 1979; The Wall of vessels in atero-and a trombogeneza, researches in the USSR, under the editorship of E. I. Chazov, M., 1983; With t r at to about in A. I. and Serov V. V. Pathological anatomy, M., 1979; Strukov A. I. and With t r at-to about in and S. M. Structurally functional bases of a hemostasis and its pathology, Arkh. patol., t. 42, No. 9, page 3, 1980; H and-z about in E. I. Fibrinferments and embolisms in clinic of internal diseases, M., 1966; H elements E. I. and Lakin K. M. Anticoagulants and fibrinolitic means, M., 1977; Chemistry and biology of thrombin, ed. by R. L. Lundblad a. o., Ann Arbor, 1977; Guthert H. u. V about 1 1-mar F. Zur Morphologie der Thromben, Folia haemat. (Lpz.), Bd 95, S. 118, 1971; Human blood coagulation haemostasis and thrombosis, ed. by R. Biggs, L. a. o., 1972; Lehrbuch der allgemeinen Pathologie und pathologischen Anatomie, hrsg. v. M. Eder u. P. Gedigk, S. 70, B., 1977; Shira-s a w a K. Electron and experimental thrombosis, Acta pat. jap., v. 16, p. 1, 1966; S t r a n d n e s s D. E., WardL a. Krugmire R. The present status of acute deep venous thrombosis, Surg * Gynec. Obstet., v., 145, p. 433, 1977
Woolf N. Interaction between thrombin and underlying artery wall, Haemostasis, v. 8, p. 127, 1979.
V. P. Baluda (stalemate. physical.).