2 Subtypes:

1. working – blood stream enforcement in organ during its function increasing (coronary circulation enforcement at heart activity enforcement, salivary glands hyperemia at food taking);

2. reactive – blood circulation enforcement after its short-termed limiting. It is usually developed in kidney, brain, skin, intestine, muscles.

Pathological hyperemia is developed under unusual (pathological) stimuli action or as a result of vessels hypersensitivity to usual stimuli. It accompanies such pathological processes as inflammation, allergy, burnings, fever. It is also expressed as rash at some infectious diseases (scarlet fever, measles and so on) or at trigeminal nerve neuralgia (one face half hyperemia)

2 main developmental mechanisms (of pathological hyperemia): neurogenic and delt with humoral factors action (myoparalythic).

Neurogenic hyperemia:

1. neurotonic – at impulsation enforcement through vasodilating nerves (parasympathetic nerves, cholinergic sympathetic nerves); experimental modeling – vasodilating nerves irritation (chorda tympani irritation leads to arterial hyperemia and mandibular salivary gland hypersecretion – Klaud Bernar experiment); under clinical conditions – at extero- and interoreceptors irritation as well as at vasodilating nerves and their centers irritation (explanation of face and neck hyperemia at pathological processes in ovary, heart, liver);

2. neuroparalythic – at impulsation stoppage through vasoconstricting sympathetic nerves; it is experimentally modeled with surgical operations and pharmacological methods; often sympathetic adrenergic fibers and nerves cutting is applied: sciatic nerve sympathetic fibers cutting led to frog leg vasodilation (Walter’s experiment) while sympathetic trunk cervical node removal led to rabbit ear rubor and hyperthermia at the operation side (Bernar’s side); following pharmacological drugs are used: ganglioblockators, sympatholithics, alpha-adrenoblockators.

Myoparalythic hyperemia causative agents:

1. inorganic ions (potassium, hydrogen) and oxygen deficiency;

2. metabolites (lactic acid, Krebs’ cycle organic acids, ADP, AMP, adenosine);

3. biologically-active substances (histamine, serotonine, prostaglandines).

Mentioned factors cause vasodilation when their direct action to vascular wall smooth myocytes or indirectly, through vessels endothelium.

Results:

1. organ metabolism and activity enforcement as a result of increased functional loading;

2. vascular wall rupture and haemorrhagia (often in brain).

31. Venous hyperemia

Venous hyperemia – organ or tissue part blood filling enforcement as a result of retarded blood outflow through veins.

Reasons - factors:

1. intravascular – vessel occlusion with thrombus or embolus;

2. extravascular – veins pressure with tumor, scar, increased tomb, oedematic fluid;

3. factors of the vessel wall as it is: elastic apparatus weakness, myocytes insufficient development and decreased tone);

4. total haemodynamics disorders (heart right ventricle function weakness, thorax absorbing action decreasing, blood stream retardation in small circulation circle).

Features:

1. organ or tissue part increasing;

2. cyanosis;

3. local temperature decreasing;

4. oeedema;

5. pressure increasing in veins and capillaries in stagnated region;

6. blood retardation;

7. erythrocytes diapedesis (exit outside vascular bed);

8. pendulum-like blood movement and stasis (at ending stage);

9. veins walls overstretching;

10. muscular tunic hyperthrophy;

11. phlebosclerosis;

12. veins varicous dilation.

Results:

1. tissular hypoxy due to arterial blood inflow limiting to organ, then to injured metabolism products action to enzymatic systems which leads to oxygen utilization disorder; hypoxy determines tissular metabolism disorders, atrophic and dystrophic changings, fibrosis (connective tissue excessive growth) for example, liver cirrhosis at venous stagnation due to cardiac insufficiency; hypoxy is local hyperemia result;

2. hard haemodynamic disorders (at generalized hyperemia) the mostly often at portal and caval veins occlusion; blood accumulation in these vascular reservoirs (up to 90% of all blood) is accompanied by blood pressure strong increasing, heart and brain dystrophy which can lead to death.