PERIPHERAL BLOOD CIRCULATION DIS

June 4, 2024
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PERIPHERAL BLOOD CIRCULATION DISORDERS.  ARTERIAL HYPEREMIA. VENOUS HYPEREMIA. ISCHEMIA. STASIS. EMBOLISM. THROMBOSIS

 

Due to the local circulation of the blood the delivery of organs and tissues by oxygen and nutrients and moving away from them of the metabolites are made.

To the local discords of the circulation blood belong:

·        arterial hyperemia

·        venous hyperemia

·        ischemia

·        stasis

·        thrombosis

·        embolism

 

Arterial hyperemia

 

Arterial hyperemia is the enhanced blood filling of an organ  because of the reinforced blood inflowing through arterial vessels.

There are the physiological and pathological arterial hyperemia. The typical example of the physiological hyperemia is work hyperemia, which develops during the reinforced organ function (muscle hyperemia at the physical training, cerebrum hyperemia at the intellectual work, hyperemia of internal organs at the digestion). Here also belongs the hyperemia of the psychogenic origin (anger, shame).

Pathological arterial hyperemia is observed when the part of body or all organism exposes to the influence of unusual factors of external or internal environment – microbe toxins, chemical substances, biologically active substances etc. there are a few types by the  mechanism of it.

Аngioneurotic hyperemia is displayed in two forms – the neuroparalytic and neurotonic types. The first one arises due to paralysis of vasoconstrictor nerves, the other one – at the stimulation of vasodilatator nerves. The neuroparalytic hyperemia is explained  by taking down of permanent іmpulsation on the smooth muscles of vessels from the alpha-adrenergic fibers, which by means of the mediator noradrenaline held the vasomotoric tonus. This can happen due  to the traumatic nerve cutting, as result  of the suppression of transmission of nervous impulses in the sympathic nodes with help of the ganglioblocators or the blockade of neuro-muscular synapses by the sympatolytics. This type of the hyperemia develops due to the damage of the sympathic nerves, which approach to the skin of upper extremities, muscles, organs of digestive tract. The hyperemia of neurotonic type frequently arises reflexly, for example in  the patients with the injury of internal organs. It’s known, that the crupose pneumonia is attended with redness of skin of face on of the same side. The hyperemia  of this type is also caused by  the physical and chemical factors – the heat, turpentine etc.

Collateral hyperemia arises in connection  with the difficulty of blood flowing in the magistral artery, the lumen of which is closed by thrombus, еmbol or is  narrowed by tumor.  Blood comes to the  bloodless place through the collateral vessels, which reflexly expand.

Hyperemia after anemia (postanemic) arises in the cases, when a factor, that pressed the artery (tumor, ligature, accumulation of liquid in cavity), quickly liquidates. For such conditions the vessels of before bloodless organ sharply expand and  become overflowed by blood what can bring about their break and bleeding. Also from the  blood redistribution in the blood streem anemia of other organs appeares. The redistributory ischemia of the cerebrum can bring about the loss of consciousness.  To avoid such complication, it is  necessary  to let the liquid out from abdominal cavity slowly.

The vacate hyperemia develops in connection with the decreasing of the barometric pressure, for example into divers  at their fast  lifting from the depth.

Arterial hyperemia is a permanent inflammation satellite.

Inflammation hyperemia. Purulent bronchitis

 

Arterial hyperemia  characterizes such  signs as

·        redness

·        dilatation of small arteries, capillaries and veins

·        arteries pulsation

·        the increasing of the volume of hyperemic site

·        rising of turgor

·        the increasing of the pressure in the vessels

·        local temperature rising

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Under the microscope the increasing of blood flowing  and of amount of functioning capillaries is visible. In hyperemic organ  the metabolism is enlarged. In the patients with atherosclerosis the arterial hyperemia can result in the negative superventions ( the vessel rupture and hemorrhage).

 

Venous hyperemia

 

Venous hyperemia is the increasing of blood supply of  and organ or tissue because of the difficulties of  blood outflow through the veins. A blood inflow under this is not altered or a bit diminished. Venous congestion is caused by such causes, as thrombosis, embolism, pressing of veins by tumor or enhanced neighboring organ. The outflow of  blood from veins of greater circle slows in insufficiency of right heart and decreasing of attracting force of thorax (exudative pleurisy, hemo- and pneumothorax).

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Venous hyperemia

 

Sharply expressed venous hyperemia of the digestive channel develops at the thrombosis of portal vein. The overcrowded  collateral veins of lower third  of esophagus and the hemoroidal veins are sharply expanded, their wall is thinned, what can  cause the  bleeding dangerous for life.

At the thrombosis of hepatic veins the venous hyperemia of liver and the fatty dystrophy of hepathocytes arise. On the cut the organ has an appearance of nutmeg – on gray-yellow background, caused by the fatty dystrophy, the red-dark blue spots are visible – these are the overcrowded  by venous blood broadened central veins of hepatic lobules. Such liver is called muscat.

Venous stagnation on the lower extremities  is observed when there is an impediment for the blood outflow by venous highways. They can  be compressed by tumour, pregnant uterus, scars. Venous hyperemia of the lower extremities  appeares  into the specialists, who are forced  to abide permanently in stand-up position. By favourable background for this is the hereditary weakness of valvular veins vehicle.

Venous hyperemia characterize the signs: 

а) redness with the cyanotic hue; cyanosys is explained by the piling up of restored hemoglobin over 30 % from general amount;

b) local decreasing of the temperature as a result of the limited inflow  of arterial blood and surplus heat emission;

c) slowing-down of blood stream;     

d) rise of blood pressure in veins dystal from the impediment;

e) the increasing of the volume of the hyperemic tissue (edema) because of the transsudation of liquid from vessels.

In case venous stagnation there is the hypoxia, a development degree of which determines the process superventions.  For conditions of anoxaemia the parenchime organs elements  die and than overgrows a connecting tissue which is more resistant to the hypoxia. Further follows a sclerosis and consolidation (іnduration ) of organs. These phenomena are known  under the names of  liver cirrhosis,  cyanotic induration of the spleen and kidneys.

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Ischemia

 

The ischemia (local anemia) is called the diminished organ or tissue blood supply because of the insufficient  inflow of arterial blood. There are  three types of ischemia by the mechanism of their beginning – compressive, obturational and angiospastic.

A compressive ischemia is the result of the  artery squeezing by tumor, scar, еxudate, ligature, bandage, foreign body.

An obturational ischemia arises at the partial or full closing of artery lumen by thrombus, еmbole, by sclerotic plaque. This form  is typical for the obliterasing endarteriitis,  when vessel lumearrows because of the productive inflammation of its wall.

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An angiospastic ischemia caused by the various chemical and biological irritants which narrow the vessels (trauma, cold, еrgotoxine). Аngiospasm can happen reflexly  at the pathology of internal organs. A typical example of such ischemia  is a spasm of coronal vessels and stenocardia paroxysms in patients with ulcerous stomach or duodenum disease, pancreatitis, cholecystitis, bile- and urine lith disease. Angiospasm is typical for all cases of the sympathic hyperactivity, and the constriction of arteries for the account of noradrenaline action on the vessel alpha-adrenoreceptors can be supplemented by the surplus formation of angiotensine ІІ.  Аngiospasm can be caused by the negative emotions such as pain, fear, anger.

The ischemia arising because of the blood redistribution from one organs to other is known separately. The cases, when an ischemia of cerebrum and the loss of consciousness were the supervention of the fast suction of ascytic liquid from abdominal cavity are known. A previous ischemia of internal organs suddenly changed on the hyperemia  for an account of outflow of blood from cerebrum. An identical phenomenon is observed at the overdosage of the vesseldilatative substances. 

An ischemia is attended with the signs, among which the most typical are:

·        pallor of the ischemizated site

·        the decreasing of its volume

·        local decreasing of the temperature

·        pain

·        the appearance of the paresthesias

A speed of blood flowing in the arterial vessels beneath the impediment is slowed, the blood pressure is low, amount of functioning capillaries is diminished.

The consequences of ischemia depend on the depth of anoxaemia. It can get through without trace or complete by the necrosis of the ischemisated site – the infarction, gangrene. There is the large possibility of the necrosis appearance,  if the ischemia comes suddenly and continues for long time. The consequences, are usually the more terrible the greater arterial trunk is turned out from  bloodflow. The ischemia in heart and brain is very dangerous. These organs are distinguished by high function level,  and thus by high need in oxygen.

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Myocardial infarction

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Gangrene

 

The kidneys, lungs, spleen are more resistant to the hypoxia but in them frequently happen the infarctions. Their microcirculative streem  is built that way,  that does not provide the proper collateral bloodflow in the conditions of  the obturation of the arterial trunk. Other organs (muscles, bones, skin) suffer from ischemia  less.

The important sense have the organic damages of arterial vessels. In patients with arteriosclerosis the infarctions arise more frequent, because the sclerosed vessels are unable to dilate adequately to needs of the blood supply. The cardiac and respiratory insufficiency, anemia contribute to infarction development.

 

Stasis

 

Stasis – this is a blood motion stop in the vessels of microcirculative stream, chiefly in the capillaries. There are three varieties  of a stasis – true (capillary), ischemic and venous.

Stasis in brain vessels

true stasis  is caused  by various factors – by cold and heat, acids, concentrated salts solutions,  turpentine. Infectious-toxic stasis appeares in extremities of patients  with louse-borne typhus. Stasis is typical also for the acute inflammation in аlergisated organism (Arthuse phenomenon ).

In the mechanism of capillary stasis main sense have the changes  of  reologic blood properties. Morphologically the stasis is expressed by the intracapillary  erythrocytes aggregation.  This phenomenon is called sladge-phenomenon. The erythrocytes stick together, forming so called “monetary сolumnes. The hemolysis and clotting of blood under this do not take place. The aggregated erythrocytes  makes resistence to the motion of blood and stop it. To the full stop precedes  the retardation of blood flow – it is the prestasic state, or prestasis. Contributes to  the development of stasis a blood condesation because  of the rise of capillary walls permeability, that happens at the  hyperemia,  hypoxia,  vasculites, the action of high and low temperatures, allergic processes.

Іschemic and venous stasis have the same causes as the processes, at which they are observed (іschemia, venous hyperemia).

 

Thrombosis

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By this term the intravital blood or lymph concertion in vessels and in heart chambers cavities is marked. A clot of blood  (lymph), that formed, is called thrombus.

The main factors of thrombforming now are well famous. These are:

·        the damage of vascular wall,

·        local angiospasm, аdhesion and aggregation of the thrombocytes,

·        slowing-down of bloodflow,

·        disturbance of balance between coagulative, anticoagulative and fibrinolytic blood systems into dominance side of the first of them.

 

The vessels wall can be damaged in result of mechanical trauma, under action of chemical agents and bacterial endotoxines, in the  inflammation, atherosclerosis, hypertensive illness. The damage of vessels frequently has the starting role. From here starts the process of thrombformation. From damaged wall throw out the substances, which activate thrombocytes, assist their adhesion and aggregation, and also to blood coagulation.

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Local vasoconstriction after the damage of tissues is conditioned by the spasm of smooth muscles of the arteriols under the influence of noradrenalin, that is excreated in the adrenergic synapses. Vasoconstriction contributes to the release  into blood of the tissue thromboplastin, and noradrenalin activates Hagemann’s factor. Thanks to the vasoconstrictioot only elementary bloodloss is limited, but the  local accumulation of hemostatic substunces takes place.

The adhesion of thrombocytes is in their ability to come into contact with deendothelised vascular wall, to connect with its receptors  with collagene fibres of basal membrane, to spread and close down the defect. The adhesion takes place double-quickly, during 3-10 с. In it,  besides the thrombocytic factors, a special plasma albumen – Vilebrand’s  factor participates.

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Adhesion of thrombocytes

 

An aggregation is a following stage of thrombforming. Parallel to the adhesion to collagene  and other subendothelial  structures the thrombocytes begin to stick together. On the spreaded thrombocytes quickly settle the other ones. So the aggregates from 3-20 thrombocytes arte generated, the amount of which quickly increases.

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Settling of the circulatory thrombocytes is made by biologically active substunces, among which the most important are two – thromboxane А2 and аdenosinephosphate (АDP). They are produced by the settled thrombocytes. Тhromboxane  А2 is derivative of the arachidone acid. ADP is thrown out from  the dense granules  of thrombocytes  together with serotonine.

 

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Pathogenesis of thrombosis

 

About the significance of slowing-down of bloodflow in thrombforming  testify the facts of principal thrombi localization in veins, on lower extremities, in places of vertical blood motion (aneurism, pockets of venous valves), in patients with cardiac insufficiency, attached to the relaxation of the attracting action of thorax, attached to the presence of local impediments for outflow of venous blood.

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By the adhesion and aggregation of the thrombocytes and by accomplishes a cell phase of thrombforming. Following phase is plasmatic, an it essence comes to the acceleration of blood clotting (hypercoagulation).

There are two mechanisms of activation of this complicated multistaged process – internal and external. An internal mechanism begins from Hageman’s factor of activation, and external is in outflowing of the tissue thromboplastine in the place of damage. Both they have one destination that is to activate a Х factor (Stuart’s-Prauer),  where upon the active thrombin is generated, and further from the fibrinogene – the  stable fibrin.

Dependency on the contents there are: white, red and mixed thrombs.

 In white prevail the leucocytes, it is generated slowly attached to fast blood motion,  in arteries.

Red thrombus contains more erythrocytes, it is generated quickly, principal in veins. The most frequently  the mixed thrombs are met, in which the leucocytes  are  in layers with erythrocytes. They are generated in heart cavities,  aneurism, varicose broadened veins.  

Червоний тромб 

 

Red thrombs 

Змішаний тромб

                  

Mixed thrombs

The thrombosis concequences may be favourable and unfavourable. The best variant is asepsis аutholysis, when a thrombus swings open for the activation of the fibrinolytic  blood system and leucocytes proteolytic enzymes. However big thrombs dissolve seldom, more frequent they extend by connecting tissue (organization of thromb). Growing in of the connecting tissue begins from the place of fastening of the thromb to wall of vessel, from the head. 

Thrombus condenses, gets dry,  the cracks are generated in it, through of which the blood motion can revive in the vessel. This phenomenon is named recanalisation. A surface of such channels are  covered by endothelium, the channels become the vessels. Organized into a thrombus extend the small vessels, which feel it – the vascularisation of the thrombe. The organized thrombs are able to calcinate, in them the veins are named phlebitis.

The unfavourable thrombosis completion is septic autholysis of the thromb,  its pyogenesis.  The reason of purulent melting of thrombus appear the particles, which are carried by blood to different organs. This conduces to the generalisation of purulent inflammation and sepsis development.  The thrombosis consequences can be the coronary thromboses, thrombembolias, thrombophlebites.

Embolism

 

The embolism is obstructing up of lymphatic or blood vessels by the particles (еmbols), which iorm in blood and lymph do not meet.

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Embolism is subdivided on exogenous and endogenous.

The exogenous embolism may be:

·        air

·        gaseous

·        bacterial

·        parasite

·        made by foreign bodies

Endogenous embolism subdivides on:

·        thrombembolism

·        fatty

·        tissue

·        embolism  by amniotic fluid

 

Air embolism is observed, as a rule, at the damage of large veins, in which  there is the negative pressure. This happens in cases of fighting or domestic wound of jugular or subclavian veins, at the pneumothorax, operations on heart, after childbearing, when the uteric veins do not close, at the accidental air introduction into vein together with medicines. Air amass in chambers cavities of right heart, drags  them apart and is brought into the vessels  of the  small blood circle. 

 

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Gaseous embolism happens at the caisson works. Steeping on the depth, man breathes in gaseous mixture under increasing pressure. Accordingly increases the gases solubility in blood. If there’s the necessity of fast diver lifting on the surface, the dissolved gases are not able to expire through the lungs and get across into gaseous state.  Blood “begins to boil. The gas bubbles,  which almost completely consist of the nitrogen, obstruct the vessels. Identical can happen at the dehermetisation of the flying аparatus. Embolism of the type complicates the passing of gaseous gangrene.

 

The bacterial and parasirte embolism is obstructing up of vessels by microorganisms, candidas, protozoon, parasites (trichinels). Frequently microbe embols are generated at the purulent thrombi melting. In obstructed places the metastatic  ulcers develop.

Embolism by foreign-bodies comes  when into the vessel’s lumen the bullets, mine splinters and other solids are brought. The heavy bodies move not far, sometimes against  the blood flow.

 

Endogenous embolism is most often caused by the thrombus, that tore off from vascular wall. 

Thromembols from veins of greater blood circle and from cavities of right heart are brought for blood motion into pulmonary artery, and that ones, that formed in the cavities of the left heart, bring on the brain infarction,  the infarctions of the the kidneys, spleen, gangrene of the mesoperitoneum and lower extremities. Lightly obrupt the thrombus, that formed on the mitral and aortic valves at the rheumatism, protracted septic endocarditis, heart defects. 

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Fatty embolism arises at the traumatic damage of hypodermic adipose tissue, fractures of long bone, in which the marrow is deputized by fatty tissue, and also at the mistaken injection of medicines, dissolved on oil, into the vessels.

 

Fatty embolism of lungs

 

Fat for the blood motion comes  into pulmonary artery. Death arises in case obstructing of two  thirds of branches  of pulmonary artery.

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Fatty embolism

 

Tissue (cellular) embolism develops at the destruction of the tissues by trauma or pathologic process. Under this the tissue pieces or cell groups come  into blood streem. The embols become the heart valves pieces at the ulcerous endocarditis, aorta wall pieces at the ulcering of the aterosclerose plaques, pieces of cerebrum at the cranial-cerebral traumas (especially into babies at the childbed  trauma), cancer cells. The last ones can extend to the veins wall and lymphatic walls, abrupt from the tumor and metastase into other organs. Here is taken the embolism by the petrificates and the amniotic waters in the pregnant women.

The embols, usually, moves down the blood stream (оrthograde embolism). Sometimes the foreign solid bodies under the influence of their own weight lowering into lower posed parts of body against  the blood motion (retrograde embolism). The retardation of the bloodflowing and relaxation of the succing force of thorax contributes to this. Into persons with the defects intraatrial or intraventricular septs   the embols can go from the  right half of the hearts into the left one and further into aorta, passing by the lesser circulation (paradoxical embolism).

Paradoxical embolism

 

The symptoms of embolism depends, foremost, on its localization. That’s why there are the embolisms of the lesser circulation, greater circulation and portal vein.

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The threatful complication is the embolism of pulmonary artery. It arises in the patients with thrombosis of lower extremities and the cavity of right heart. Embolism of greater circulation reverberates on the structure and function of the organs, into which the embols are brought.

Емболія легеневої артерії

Embolism of pulmonary artery

 

Violation of microcirculation and blood circulations in area of inflammation

 

The possibility of the necrosis depends on the development of the degree of collaterals and reflex spasm of the obturated  and  remoted vessels. The major pathogenic link of the embolism of the portal vein is syndrome of the portal hypertension. The internal organs are overflowed by blood, a liquid percolates into the abdominal cavity (аscytis). The  spleen is enlarged (splenomegaly). The superficial veins of the front stomach wall are widened. From the superficial veins of the esophagus and stomach the bleedings are possible. The effects of arterial hyperemia are the increase of blood flow speed, the increase of functioning capillaries amount, and the rise of blood pressure, strengthens of the tissues oxygenation.

Arterial hyperemia

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Arterial hyperemia promotes the derivation of the oxygen radicals for the protection of the organism against the microorganisms, forming of humoral plasma factors of the organism protection (complement, properdine, fibronectine), causes the movement of leucocytes into the area of injury. Arterial hyperemia causes the redness and warmth of the injurious area.

Venous hyperemia is characterized by the deceleration of blood circulation, the change of blood viscosity (it’s a result of exudation), and the  chaotic placement of blood cells. Blood becomes very viscous; erythrocytes swell and move slowly, sometimes they stick in capillaries.

The development of venous hyperemia is promoted by three groups of factors:  І – intravascular, ІІ – vascular, Ш – extravascular.

 

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Intravascular factors are follows: erythrocytes swelling and blood viscousness, which are the result of the increase vessels permeability; the forming of mycrothrombuses, the disposition of the leucocytes near the vessel wall.

Vascular factors: the development of venous hyperemia is promoted by the increase of endoteliocytes sizes and as a result the diameter of capillaries decreases. The elasticity of venal and lymph vessels decreases as a result of collagen and elastine destroy caused by lysosomic enzymes. Extravascular factors: edematic fluid easily squeezes vessels and deepens the violation of blood circulation.  Venous hyperemia, which lasts very long time, creates conditions for the development of prestasis. The movements of blood are similar to the movements of a pendulum: blood moves from arteries to veins during systole of the heart and comes back during  diastole of the heart.

The increase of blood viscosity, platelets aggregation cause the development of stasis, which is characterized by the stop of blood movement, swelling and aggregation of erythrocytes and their destruction. Changes of the erythrocytes membrane cause the aggregation of erythrocytes. The erythrocytes during the inflammation becomes swollen; the decrease of the blood albumins amount, as the result of the amplified penetration of blood plasma out the vessel,causes the decrease of negative charge of membrane erythrocytes  and their conglutination.

Lymphatic system also participates in mechanisms of the inflammation. In a healthy organism lymphatic system executes the drainage function. Their major functions are the extract of microparticles, macromolecules, detritus of the cells and the exchange of liquid between blood and tissues. The inflammation involves many sites of lymph system. Edematic liquid compress lymph capillaries and changes local lymphatic circulation. The damage of cells membranes breaks the pump function of lymphatic collective vessels. The inflammation is accompanied by the increase of lymphatic capillaries permeability and their overflow. The detritus of the damaged cells and proteins get into lymph. The injurious factors can cause the inflammation of lymphatic vessels and lymphatic nodes. Due to the drainage function of lymphatic system the amplification of lymphcirculation promotes the decrease of swelling and carry antigens to the lymphatic nodes. Besides the amplification of the drainage function of lymphatic vessels can promote the distribution of the infectious agent and the toxic products of proteins disintegration. Spasm of the lymphatic vessels, which usually arises proximately from the area inflammation and inflammation of the lymphatic nodes deepen the swelling in the area inflammation and evidence development of lymphatic circulation insufficiency. The principal value of the alteration and violations of microcirculation is the creation of unfavorable conditions for further penetration of the pathological agent into the organism.

Exudative and proliferative processes

The increase of vascular wall permeability provokes exudation (penetration of a liquid from the blood into the tissue), emigration of leucocytes.

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The permeability of microvessels increases first of all (especially of venules). The amplification of exudation provokes: of reologic properties blood change and microperfusion as the result of blood condensation; of laminar blood stream violation; of plasma structure change after the output into the tissue proteins; of microvessels compression by the edematic liquid. These processes provide of phagocytosis (protective process); it is sufficient activity and restoring of the injury tissue. In a stage of arterial hyperemia and especially in venous hyperemia stage fluid with the proteins and salts, dissolved in it, penetrates out the vessel. The high hydrodynamic pressure in vessels and the low colloid-osmotic pressure of blood increase of the vessels permeability and penetration of plasma proteins into the tissue.

There are three ways penetration of fluid through the vessel wall (exudation). The 1st way is interendotelial (betweeearby endotheliocytes). Histamine promotes contraction of endothelial cells, the slots betweeearby endotheliocytes extend, and basal membrane is exposed. The second way of exudation is transendotelial (through the endoteliocytes cytoplasm). Vesicles pinocytosis activity (the catch of fluid) of the endoteliocytes increases. The blood plasma is inside vesicles, which move through the cell and some time form channels. Various substances can pass without any control through channels (microvesicle transport). The third way of the exudation is the vessels wall area, where are injure endoteliocytes.

The development of the inflammation promotes the amplification of the exudation and the output of blood plasma and the mediators outside the vessels. The main cause of the exudation is mediators of inflammation, but amplifying disorder of the metabolism, the injury cells and leucocytes promotes other pathological mechanisms, which increase vascular permeability. They are lysosomes hydrolytic enzymes of various phagocytes and parenchimal cells (collagenase, elastase) and bacterial enzymes (hyaluronidase), lactic acid and piruvate acid, another non-oxidated substances, which are the result of tissues hypoxia, adenosine, Н+ and K+, especially during the decrease of Са2+ level.  First of all albumins, than globulins and fibrinogen, which promotes the formation of fibrins clots, penetrate outside the vessels.

The serious damage of vessels wall is accompanied with the erythrocytes diapedesis (penetration through the vessel wall) and the bleeding.

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The exudation peculiarity and its structure depend on osmotic, oncotic and hydrodynamical factor of inflammation. Hyperosmia (high osmotic pressure) and hyperoncia (high oncotic pressure) of the tissue in the area inflammation) and osmotic-oncotic pressure of blood are differed, so fluid penetrates out the vessels and amplifies swelling. Hyperosmia is the result of the accumulation osmotic active particles (K+, Na+, salts, light-weight organic substances) of injurious tissue. Hyperoncia is the result of the macromolecules disintegration substances of the injurious tissue accumulation.

INFL031

 

There are three types of microvessels permeability change. The first type is the, second type – immediate-continuous, third type – deferred-prolonged increase of permeability of walls of vessels during inflammation. The first type is called the immediate-transient and occurs during weak damages. The main cause of it is the release of histamine, serotonine, and bradykinine. The contraction of endothelial cells and extension of interendothelial slots in small and average venue occurs under the influence of histamine. The permeability of walls of capillaries does not change. Endothelial cells of small and average venue have more histaminic receptors, than the similar cells of capillaries and arterioles; therefore only venue are involved in the process of such type.

The second type of vessels permeability violation arises during hard tissue damages (for example, extensive serious burn). The sharp increase of microvessels permeability arises immediately after damage and lasts up to five day, because endothelial cells of microvessels perish and is characterized by plasmorrhea.

The third type of vessel permeability changes is characterized by the lasting latent period after the damage. After that the permeability of vessels sharply increases and last for some hours or days. This type of vessels response is the most frequently with the human being (thermal damages, tissues injury by ionizing and ultra-violet rays, operation of bacterial toxines, delayed type of the allergy). In these cases endothelial cells don’t round, but juncture between endotheliocytes of the capillaries and venules is broken. The combination of several mechanisms in dynamics the inflammation is possible.

Amplified exudation promotes the development of edema, pain and the function violation. The pain is the result of the nervous ending compression caused by exudates. The violation of the organ or tissue function is the result of the increase of diffuse distance between the capillary and parenchymal cells, and also their compression. The exudation deepens negative effects of the inflammation: the disorder of metabolism and microcirculation of the injurious tissue, hemoconcentration, derivation of thrombus. But at the same time the pathological factor operation weakens due to injuries area.

Vascular changes and the blood stream deceleration promote the reallocation of blood cells: leucocytes move to the vessel wall and begin to attach to it. Then, leucocytes adhere on the endotheliocytes and form the cover along the vessels walls.

 

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The process of the edge standing of leucocytes is necessary two following conditions: the increase of endothelial cells adhesive properties and the activation of leucocytes.

 

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The increase of adhesive properties of endotheliocytes is promoted by the lowering of their negative membrane charge (it’s the result of the accumulation in the area of inflammation Н+, Ca2+, Мg2+, Mn2+, cationic proteins, excreted by activated leucocytes). These ions reduce the leucocytes negative charge too, and also activate leucocytes enzymes, which increase adhesive properties of these cells.

Complement, fibronectine, immunoglobulins, histamine, interleukines, leucotriens are the most important initiators of the activation of leucocytes adhesive properties. C5, IgG (Fc-fragment) and IL-8 (chemotactic factors) promote the activation of these cells and their movement to endotheliocytes. Gradually leucocytes begin to pass through the vascular wall and to emigrate into the tissues (positive chemotaxis).

The penetration of leukocytes through the vessels wall is promoted by the alteration of leukocytes, endotheliocytes, interendothelial contacts basal membrane and perivascular tissue states.

 

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After the adhesion of the leukocyte to the endotheliocytes membrane it moves on its surface and goes to the interendothelial slot. The leukocyte forms a pseudopodium, which moves through the interendothelial slot into the underendothelial space.

 

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All contents of leukocyte move into the pseudopodium, and the leukocyte places in between the endothelial cells and the basal membrane of the microvessel. Then the leukocyte excretes collagenase and elastase, partly alters basal membrane and passes through the vessel wall and gets out the vessel.

In most cases of acute inflammatioeutrophyles emigrate the first (that process lasts 6-24 hours). In 24-48 hours monocytes emigrate most actively. Lymphocytes emigrate a little bit later. Lymphocytes can immigrate the first during virus infection and tuberculosis, and eosinophiles – during allergic reactions. Leukocytes regulate of the cells cooperation and delete the alien agents or the detritus of defective tissues. The neutrophiles (microphages) destroy pathological agents due to the following properties: the absorption of the foreign agent (phagocytosis), the microbicydity and cytotoxicity (these are the mechanisms of the foreign agent destroy by such biooxidants as superoxide anions, hydroxyl- radicals, singlet oxygen, peroxide), the intra- and extracellular lysis.

The neutrophiles excrete the proteolytic enzymes and oxidants into the phagosoma and destroy pathological agent. The excretion of proteolytic enzymes, biooxidants, thromboxans, prostaglandines, leucotriens out the neutrophiles promotes a self-regulation of the inflammation.

The main functions of the monocytes (macrophages) are the phagocytosis of foreign agent or damaged tissue and the immune reactions stimulation. The high-specifically phagocytosis of the foreign object is carried out due to the electrostatic interaction forces, and especially due to the membranes receptors for Fс-fragment of immunoglobuline G and СЗ component of the complement system, which taking part in a destruction of foreign agent too. The fastening and phagocytosis of the microorganisms promotes stimulation of macrophage, its oxidizing processes and secretion of the bactericide products (lysosomal enzymes, cationic non-enzyme proteins). But some of the particles, especially the inorganic ones, can be stable against such effect and even can cause damage of macrophage. So, the condition of the impossibility of pathological agent elimination is created. In such situation the macrophages execute their protective function in another way: they surround the hard-phagocytible particles and form a cellular conglomeration–node or a granuloma. The macrophages also excrete the factors, which stimulate or inhibit the cellular prolipheration and regulate the regeneration processes (tissues structure restoring).

The lymphocytes play the main role during virus infections. The mowing of lymphocyte out the vessel is promoted by substances (monokines), which are secreted by blood and tissues macrophages. The cooperation of T- and B-lymphocytes with phagocytes   is necessary for immune reaction stimulation and phagocytosis activation with the involvement of complement system. All inflammation effectors cells have Fс-receptors of immunoglobuline G and C- receptors of complement.

 

Types of exudates

 

The inflammation is named the exudative if this component is expressed stronger than others. The exudate type determines type of an inflammation. There are serous, fibrinous, purulent, decaying, hemorrhagic and combination types of the exudates and inflammation. The serous inflammation develops in mucous and serous coats, interstitial tissue, skin, and kidneys glomes capsules. The amount of cells in the serous exudate is not large.

The serous exudate promotes washing off of microorganisms and their toxines from the damaged surfaces. But the serous exudate in brain coats can squeeze the brain and violate its function. The serous infiltration of lungs alveolar septs can cause the development of acute respiratory insufficiency syndrome.

 

 

The fibrinous exudate contains a plenty of fibrinogen, which forms clots of fibrin in tissues. Such inflammation occurs when an organism is affected by corinebacterium diphtheriae, pneumococcus, Fridlander’s bacillus, Frencel’s diplococcus, streptococcus, and mycobacterium of tuberculosis. Such type of an inflammation occurs on mucous or serous coats more often.

 

 

The causes of purulent inflammation are staphylococcus, streptococcus, gonococcus, meningococcus, and Frenkel’s diplococcus.  Purulent exudate consists of many viable leukocytes and purulent bodies (perishing leukocytes), cells detritus, microorganisms, plenty of proteins (especially globulines).

 

 

1

2

 

Fig. Pural bodies (destroing of neutrophyle – 1, destroing of monocyte – 2)

 

The decaying inflammation develops after the invasion of decaying microflora into the purulent inflammation site. During this type of inflammatioecrosis of injurious tissues progresses, the inflammation area doesn’t localize, and this provokes the arrival of alien and toxic products into vessels and the development of intoxication due to which the patients usually dies.

1

 

The hemorrhagic inflammation, as the form of the serous, the fibrinous or the purulent inflammation, is characterized by erythrocytes impurity to the exudate   (Siberian ulcer, natural smallpox, influenza).

The combination forms of inflammation are characterized by connection of one type of exudate to another. Any combinations are possible. Such forms usually develop as the result of connection of a new infection to the lasting process. The tissues damage and the process of inflammation cause the restoring of broken structure and function (reparative regeneration).

Inflammation. phenomenon exudative. the sorts of exudates

The inflammation proliferative phase is simultaneously a phase of the reparatory regeneration. The restoring of the damaged tissues structure depends on the interaction of connective tissues cells among themselves (fibroblasts, macrophages, labrocytes, lymphocytes, endotheliocytes), on the interaction of connective tissues cells with the intercellular matrix (collagen, proteoglicans, fibronectine), on the interaction of connective tissue cells with blood cells and parenchymal ones.

 

 

The process of cells proliferation is regulated by substances, which can stimulate (mitogens) or oppress (keilones) the reproduction of cells. Cambial cells are the tissues source of regeneratory material. The damage of tissues causes intensive proliferation trunk cells. The reparative stage of inflammation begins when phagocytes actively swallow the microorganisms or the tissues detritus. At that time labrocytes activate interaction with macrophages, fibroblasts, and intercellular matrix, clotting blood system and promote the excretion and the synthesis of substances, which stimulate proliferative processes.

Thrombocytes produce substances, which strengthen the proliferation and the chemotaxis of fibroblasts to the injurious area: the thrombocytal factor growth of fibroblasts, the factor of epidermis and fibroblasts growth, the peptide, which activates connective tissue etc.

The labrocytes excrete histamine and leucutrien В4, which activate fibroblasts proliferation. The neutrophiles excrete peptide, which activates the growth of fibroblasts and leucotrien, which cause the migration of fibroblasts into the injurious tissue.

The macrophages are the main cells, which regulate the reparative processes. Macrophages enclose (segregate) of the injurious tissue, form neutrophile-macrophagal, macrophagal and macrophagal-fibroblasts barriers – the granulating tissue.

The macrophagal-fibroblastic interaction conduces migration, proliferation, and differentiation of fibroblasts, synthesis and secretion of collagen and other components of tissues matrix. The accumulation of fibroblasts in the inflammation site inhibits their growth and stimulates the biosynthesis of collagen. Fibroblasts contact interaction stimulates the production of keilons.

The macrophages, lymphocytes, neutrophiles produce the intercellular matrix (collagen, fibronectine). The further stage of connective tissue growth autoregulation is characterized by the collagen synthesis inhibition, the destruction of the majority cells, the transformation of the fibroblasts in fibrocytes (inactive cells). The fibroblasts destroy unnecessary collagen fibres by means of their phagocytosis, or the secretion of collagenase. All of these promote the stop of connective tissue growth.

Granulous tissue

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 Young connective tissue with lot of vessels

This tissue covers of wound and ulcer skin defects, it is formed during the damage of mucous membranes and internal organs, during bones fractures, hematoma organization, at necrosis (infarction), and during chronic inflammation.

FUNCTIONS:

covering of defect

trophy (microcirculation regulation, oxygen and metabolites transport, filtering of substances)

morphogenetic (influence on epithelium and muscular tissue differentiation).

incapsulation (closing) of necrosis area and alien bodies

reconstruction of anatomic and functional structure of injurious tissues

 GRANULOUS TISSUE  –  one of the very important products of inflammatory-reparative process is, this is a young connective tissue with a plenty of vessels. This tissue fills wound and ulcer skin defects, it is formed during the damage of mucous coats and internal organs, during bones fractures, hematomes organization, at necrosis and infarctions sites, and during chronic inflammation. The functions of granulation tissue are as follows: mechanical (filling of defect), trophic (microcirculation regulation, oxygen and metabolites transport, filtering of substances), morphogenetic (influence on epithelium and muscular tissue differentiation). But the main function of the granulation tissue is the protection against unfavorable influences of the external environment, against infection and intoxication, incapsulation (closing) of necrosis area and alien bodies, and also reconstruction of anatomic and functional structure of injurious tissues. During the proliferative processes activation, the cells, which are constantly stimulated by mitogens, become very sensitive to carcinogenic substances. Abnormal mitosis can lead to tumour formation.

The course of inflammatory reaction depends on the organism reactivity, on the nervous, endocrine and immune systems condition. The meaning of the nervous system in the dynamics of the inflammation proves to be true by numerous cases of inflammation sings development in the patients under the influence of suggestion during hypnosis. The occurrences of hyperergic inflammation during the local action of the damaging factor at maniac excitement are often in psychiatric clinic, and at serious depressions the inflammatory reaction proceeds very languidly. The change of nervous – impulse and nervous – trophic influences on the damaged tissue promotes the amplification of exudative processes and the violation of microcirculation.

Neuromediators and trophogens, activate the phagocytosis and the free-radical processes. The violation of afferent innervation strengthens alteration processes and decelerates the reparation of parenchymal cells. Proliferative processes pass most actively on the periphery of the inflammation area, because just there nervous fibres regenerate first and anabolic processes on the periphery proceed more actively.

Neuropeptides take active part in the regulation of proliferative-regeneratory processes in tissues of organs, especially the opiod peptides. The stimulation of C-fibres opioid receptors by these peptides weakens the pain, reduces the release of noradrenalin from sympathetic nervous endings, the activation of labrocytes and trombocytes stops, the disorders of microcirculation and violation of hemostasis are eliminated.

The influence of endocrine system on the inflammation is proved by numerous clinical observations. Hyperthyroidism amplifies manifestations of the inflammation and hypothyroidism is characterized by the insignificant sings. Mineralocorticoids promote the development of inflammatory reaction and glucocorticoids weaken it. The ability of glucocorticoids to weaken the inflammation is constantly used in clinics because they reduce the amount of tissues basophiles, increase the activity of histaminase (enzyme, which destroys histamine), reduce serotonine formation, stabilize lysosome membranes and inactivate their enzymes. Glucocorticoids induce synthesis of proteins, which block prostaglandines and leucotriens synthesis. Mineralocorticoids are capable to strengthen the exudation, to accelerate the reproduction of cells, the derivation of new capillaries, and synthesis of the connective tissue.

The inflammatory reaction in the process of phylogenesis has arisen as a protective response of the organism of hot-blood biological individuals. The organism protects itself from the influence of the pathological factor due to limitation of the inflammatory area from the whole organism. The barrier is formed around the inflammation area; it allows various substances to flow in one direction (to the centre of the inflammation site) due to blockade of lymphatic and blood vessels. The unfavorable conditions for microorganisms are created in the centre of the inflammation. But in the conditions of significant tissues damage or microcirculation violations, the hard metabolism disorder in the damaged tissue or organ, hypoxia and the common intoxication strengthening patient’s sufferings can be provoked. The inflammation is the example, which connects both the elements of injury and the elements of organism protective forces.

 

 

 

 

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