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28. Stress-inducing and stress-limiting systems. Diseases of adaptation.

Adaptation diseases- diseases dominant role in the development of which has excessive stress and so-called stressor injuring mechanisms. Stress at its big intensivity and duration can be transformed from adaptation mechanism to dysadaptation and even pathogenesis mechanism. Adaptation diseases:

  1. psycho-somatic diseases:

    1. heart ishemic disease;

    2. hypertonic disease;

    3. stomach and duodenum ulcer disease;

  2. substances exchange diseases (diabetes mellitus);

  3. allergic and inflammatory diseases:

    1. bronchial asthma;

    2. rheumatism.

Stress-triggers or stressors:

  1. trauma;

  2. coldness;

  3. pain;

  4. emotions (negative ones);

  5. bleeding;

  6. physical loading;

  7. hypoglycaemia;

  8. infections.

These stressors cause excitement of the highest nervous regulatory centers and hormones big amount releasing determined by this. Such excitement can be realized through homeostasis disorders.

Stress-realizing processes:

  1. activation of hypothalamic-adenohypophyseal system – ACTH, STH, TTH releasing which stimulate (correspondingly) secretion of glucocorticoids, somatomedines, thyroid hormones;

  2. vegetative nervous system activation (sympathetic and parasympathetic) – is accompanied by catecholamines, insuline, glucagons passage to blood;

  3. aldosterone-vasopressine system activation which leads to angiotensine, aldosterone, ADH content increasing in blood.

Stress-limiting systems:

  1. endogenic opiates;

  2. lovely job;

  3. active sexual life;

  4. joy from life and so on.

29. Concept of “local microcirculatory disorders”. Some mechanisms.

Mai local microcirculatory disorders:

  1. arterial hyperemia;

  2. venous hyperemia;

  3. ishemia;

  4. stasis;

  5. thrombosis;

  6. embolism.

Endotheline is considered “maestro of blood circulation” because it plays one of the most essential role in hypertonic disease (together with atrial sodium-uretic factor). Endotheline is synthesized by endotheliocytes. Endothelium is considered now whole separate endocrine gland because all endotheliocytes weight is approximately 5 kg in 1 organism and because is a source of about 50-100 different substances influences on vessels tone, haemostasis, transcapillary exchange (and, thus, inflammation development). Endotheline is very powerful vasoconstrictor and proaggregant.

NO is its antagonist because it is vasodilator and antiaggregant. It is also can be produced by endothelicytes.

Inreased hyperemia can be caused by NO hyperproduction. Endotheline hypersecretion and hyperactivity can lead to ishemia and stasis (as a result of vasoconstriction), thrombosis (as a result of hyperaggregation). NO is also named as endothelial relaxation factor. It acts to vascular wall smooth myocytes and causes their hyperpolarization (endothelin causes depolarization) that lead to vessel basal tone decreasing and vasodilation at blood pressure action (edotheline action leads to vessel basal tone increasing and vasoconstriction). NO is origined from arginine. Both NO and endothelines act through cAMP (more endotheline) and cGMP (more NO).

30. Arterial hyperemia

Arterial hyperemia – organ or tissue blood filling increasing due to blood excessive passage to arterial vessels.

Functional features:

  1. shine arteries, veins and capillaries dilation;

  2. blood stream acceleration in them;

  3. shine arteries and capillaries pulsation;

  4. increasing the amount of vessels visible with eyes;

  5. pressure increasing in arterioles, capillaries and veins.

As the result of these functional changings one can see visual expressions:

  1. dispersed (disseminated) rubor (reddish colour);

  2. local temperature increasing;

  3. hyperemized locus volume increasing;

  4. tissular turgor increasing;

  5. metabolism and organ function enforment.

Reasons:

  1. physical factors;

  2. chemical factors;

  3. biological factors;

  4. loading increasing to the organ or tissue locus;

  5. psychogenic actions.

Physiological hyperemia – occurred under usual physiological stimuli (loading increasing to organ, psychogenic stimuli) action.

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