peripheral microcirculatory blood circulation (arterial hyperemia)

Peripheral blood circulation

• maintains the balance of nutrient substrates gases metabolites electrolytes and water in "blood tissue blood”system

• Main disorders are arterial, venous hyperemia, ischemia, stasis, thrombosis and embolism

Arterial hyperemia

An increased volume of blood in a tissue or organ due to excessive arterial inflow and normal venous outflow

Its an active process

Arterial hyperemia occur when

• When arterial dilatation produces and increased inflow of blood into capillary beds w opening of inactive capillaries

• Neurogenic mechanism or vasoactive substance release lead to arterial hyperemia

Classification of arterial hyperemia

1. Physiological

• functional

• Protective adaptive (reactive)

2. Pathological

• neurogenic

-neurotonic

-neuroparalytic

• metabolic

Physiological arterial hyperemia

• adaquate o stimulus and has an adaptive value

1. Functional: develop in organs and tissues due to an increase in their functional activity hyperemia in a contracting muscle

2. Protective-adaptive:Develop as a part of protective reactions in area of inflam, around a transplant, in post-ischemic regions. It delivers oxygen metabolic substrates , immunoglobulins and cells necessary for tissue repair

Pathological arterial hyperemia

• not adequate to effect and not assoc w a change in the function of organ-tissue has a disadaptive damaging role

Examples of pathological arterial hyperemia

• brain in hypertensive crisis

• In abdominal organs after evacuation of ascitic fluid

• Skin and muscle of limbs after removing bundle

• In zone of chronic inflammation

• On skin after severe or long lasting heat exposure

• In region w sympathetic denervation

Etiology (nedenleri) of causative factors

1. Mechanical

2. Physical (high temp, local reduction of atmospheri pressure)

3. Chemical (organic inorganic acids, alkali alcohol aldehyde)

4. Biological active susbstances (bas) formed in body (adenosine. Acetylcholine, prostacycling,nitric oxide)

5. Social (emotions ,stress in human)

Etiology by the origin can be exo-endogenous

1. Exogenous: from environemnt include infectious organsms and non infectious factors

2. Endogenous: formed in body

• depostition of concrements in tissues of kidney liver subcut tisue

• Formation of excess BAS cause a decrease in arterioles tone (vasodilation) they are: adenosine, prostaglandins, kinin accum of organic acids (lactic, pyruvic, ketoglutaric)

Pathogenesis (hastaligin nasil olustugu)

• neurogenic

• Metabolic

Neurotonic hyperemia

• due to activation of neurotonic mechanism that lead to vasodilation

• Parasympathetic nerve fiber innervate only vessels of brain, tongue, salivary gland, external ganglia, bladder and rectum neurotonic arterial hyperemia possible in this organs

• Coronary vessels of heart,cerebral arteries , mucous cheeck , small intestine innervated by sympathetic nerves exitation of them can also cause hyperemia (sympathetic vasodilators)

Caluda bernard

• reproduced it by stimulation of chorda tympani (branch of facial nerve) containing parasympathetic vasodilating fibers

• In vessles that dont have parasympathetic innvervation hyperemia caused by sympathetic system

Sympathetic system causing hyperemia

• sympathetic system ( choligernic, histaminergic, betapadrenergic mechanism) contain

• Sympathetic cholinergic nerves dilatesmall arteries and arterioles of skeletal muscle, facial muscle , mucous membrane of cheecks, intestine

• Acetylcholine is the mediator

Neuroparalytic arterial hyperemia

• occur when tone of vasoconstrictor centers and nerves decreases

• Observed after cutting the vasoconstrictive fibers and nerves(sympathetic a-adrenergic ones)

• Norepinephrine is the mediator

Neuroparalytic arterial hyperemia

• is the hyperemia that occur after ischemia

• In case of ischemia oxygenation of tissues and vessels impaired due to paralysis of the neuromuscular apparatus of vascular wall, they lose their tone

• After ischemia cessation blood begin to flow into this area but because of reduced tone of vasoconstrictors the arteries sharply expand

Neuroparalytic arterial hyperemia

• also obtained chemically by blocking the transfer of central nervous impulses to sympathetic ganglia (W help of ganglion blockers)

• Or at the level ol sympathetic nerve endings (w help of sympatholytic or adrenolytic drugs)

• Neuroparalytic mechanism of arterial hyperemia partially underlies inflammatory hyperemia, uv erythema and others

Neuroparalytic arterial hyperemia

• frosty blush on cheeck manifestation of it and initially theres a neurogenic spasm

• When skin temp fall below 15 dermal vessels begin to expand due to cold paralysis of neuromuscular excitability and conduction

Classic example of expremental reproduction neuroparalytic arterial hyperemia

• is claude bernards experiment

• Hyperemia on a rabbits ear skin on the side of cutting cervical node of sympathetic trunk

Metabolic arterial hyperemia

• caused by biological active substances of a different origin (cellular and plasmatic)

• ATP, ADP, adenosine, nonorganic ions, reduction of pO2 and increase of pCO2 in blood and tissue has the same affect

• In prostaglandins E, A that have vasodilative effect induce hyperemia

Manifestations (clinical symptoms)

Can be

• morphological( macroscopical microscopical)

• Biochemical(metabolic)

• Functional

• Clinical

Hydrodynamic pressure in arterioles capillaries and veins is increased.

Arterial hyperemia always accompanied w enlargement but never edema

Clinical manifestations

• redness of effected part

• Enlargement of organ tissue

• Local hyperthermia

• Intensificattion of organ function

Subjective unpleasent sensations can be:

• Pulsation

• Swelling

• Pain

Microscopical characterises

• dilatation of small arteries, arterioles, veins, capillaries

• Increased no of functional vessels

• Acceleration of blood flow

• Opening of inactive capillaries

Metabolism intensifies locally dues to increased supply w o2 and substrates

Significance

• in most cases accompanied w intensification of metabolim and organs function

• Has an adaptive and positive effect on inflammatory process

• Can be unfavorable

• Dilation of sclerotic vessels result in rupture and hemorrhage its very dangerous in brain