41. Microvascular tone disorders.

NO, histamine, bradykinine, noradrenaline action (through beta-adrenoreceptors) – vasdilation;

Endothelines, adrenaline action (through alpha-adrenoreceptors) – vasoconstriction.

Some organs have no any sympathetic innervation and risk of hyperemia is increased in them (sexual organs, tongue, pia mater).

Sympathetic adrenergic fibers (postganglionary) in sweat glands are cholinergic ones which increase risk of hyperemia and vascular basal tone dereasing.

Hypercalciemia can lead to vascular tone increasing.

Molecules of adhesion and transcapillary transport: adhesines, integrines, selectines (E – endothelial, L- leucocytic, P – patelet which determines substances transport on cellular surface and through endotheliocytes and thus influencing on vascular tone), cadherines, of immunoglobulins superfamily, of lymphocytes homing (directed transport to necessary places for fighting the “enemy” and in opposite direction after “war”).

Cytokines.

Fibroblasts growth factor leads to vascular wall fibrosis, atherosclerosis and vascular tone inreasing.

Hydrogen protons increased number in blood lead to vascular tone decreasing and their releasing enforcement ouside the vessel.

Oncotic pressure reducing (lower than 20-30 mm. watery column) can lead to vessels tone decreasing.

42. Extravascular disorders.

Extravascular disorders – intercellular flow (outflow) retardation and often (due to this) liquid volume increasing in extravascular space as a result to blood flow prevention to lymphatic vessels and venules. Intercellular liquid volume decreasing is observed more seldom (at dehydration or lymph production weakening) which can also been combinated with its velocity decreasing.

Reasons: local pathological processes:

1. inflammation;

2. allergy;

3. tumor growth;

4. neuro-trophyc dystrophy.

Main factors:

1. intercellular fissure constriction (particularly because of cells swelling);

2. liquid viscosity increasing (at proteins, lipids and metabolites content increasing in it);

3. lymphatic capillaries embolism and liquid resorbtion decreasing in them from intercellular space;

4. water resorbtion efficacy decreasing in postcapillaries and veins;

5. filtrational pressure decreasing in arterioles or liquid reabsorbtion increasing in veins;

6. normal and injured metabolism products, ions, biologically-active substances are accumulated in tissues; transmembrane transfer of oxygen, carbonic dioxide, substrates, ions and metabolism products is injured;

7. cells are swelled.

Syndrome of capillary-trophyc insufficiency (at prolonged course of disorders):

1. intercellular liquid flow as well as lymph and blood perfusion (through microvessels) disorders;

2. oxygen, carbonic dioxide, substrates and metabolism products exchange disorders;

3. cellular metabolism disorders.

Results:

1. dystrophic changings in organs and tissues;

2. plastic (anabolic processes disturbances in them);

3. vital activity disorder in them.

43. Concept of inflammation. Aethiology.

Inflammation is a typical pathological process, which occurs as a result of tissue injure and is expressed in complex of structural, functional and metabolic disorders as well as microcirculation disorders.

Why inflammation is considered to be typical pathological process?

General regularities of inflammation development are always expressed independently on its reason, location, organism type and its individual peculiarities.

Inflammation can appear in different organs and tissues (angine, pneumonia, appendicitis), its reasons can be mechanical trauma, temperature influence, viruses, bacteria et al.; it can be developed both in animals and human beings. Inflammation has its own distinguishing features at any concrete case. But there is common which is always expressed. This common is an inflammation essence as typical pathological process.

Flogogenic (causative) factors:

1. a) physical (mechanical, thermal, ionizing radiation, ultraviolet irradiation et al.);

b) chemical (acids, alkalis, hard metals salts, phenols, aldehydes et al.);

c) biological (viruses, bacteria, protozoa);

2. Exogenous – coming to organism or acting from external environment:

   1. infectious (bacteria, viruses, parasites, protozoa);

   2. non-infections (mechanical trauma, thermal, electrical, radiation stimuli; acids, alkalis; side proteins, insects toxins; psychogenic factors).

3. Endogenous – they are formed inside the organism:

   1. tissues decomposition products,

   2. malignant tumors,

   3. thrombi,

   4. infarction,

   5. haemorrhagias,

   6. salts accumulation,

   7. biliary acids,

   8. saprophyte microflora et al.

It is necessary to remember that at first meeting flogogenic stimulus force is very important (law of stimulus force or fore correlations is working): the more stimulus force is, the more acute is inflammation course (up to definite limits). But inflammation character, course and result is determined not only by stimulus peculiarities but also conditions in which it acts (first of all – organism reactivity).

Dependently on organism initial state inflammatory reaction expression can be different. At adequacy of organism answer reaction to flogogenic stimulus action force normergic inflammation is developed. At organism hyperreactivity – hyperergic inflammation, at organism hyporeactivity – hypoergic one.