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sections
microcirculation
functional organisation of microcirculatory units
organ related to specification of capillaries
control of microcirculation
microcirculation
flow of blood within the smallest vessels. These vessels are embedded in the organ tissues. The microcirculation is made of the arterioles, capillaries, and venules, terminal lymphatic cells.
functional organisation of microcirculatory units
Arterioles- branch off arteries
innervated by the sympathetic adrenergic fibers and they are highly responsible for the sympathetic vasoconstriction
The rhythmical contraction and the relaxation of the arterioles occurs, spontaneously via spontaneous vasomotor.
capillaries one cell thick for diffusion
There are 3 main structural classifications: fenestrated, discontinuous and continuous
The capillaries are known for their high surface area and high permeability, to fluid and macromolecules
primary site of the exchange for fluid, electrolytes gases and macromolecules.
venules
The sympathetic innervation of the large venules alters the venular tone, which regulates the hydrostatic pressure.
Terminal lymphatic vessels
The spontaneous and stretch activated vasomotion acts as a “pump” to the lymph.
The sympathetic nerves cause contraction.
have one-way valves direct lymph from the tissue and back to the systemic regulation via the thoracic duct and subclavian veins.
types of capillaries and their specific organs
Continuous- e.g. muscle, skin and lung and CNS --- uninterrupted lining, for the small ions (water, ions) to pass through
Fenestrated e.g. exocrine glands and intestinal mucosa --- small pores (fenestrae) in walls so more permeable and allow small proteins to diffuse.
Discontinuous/sinusoidal e.g. in the liver, spleen and bone marrow. large gaps between endothelial cells and a discontinuous basement membrane, allowing even blood cells and large proteins to pass through.
control of microcirculation
neural control - SNS releases norepinephrine which binds to alpha receptors causing vasoconstriction
Hormones - angiotensin ii and vasopressin cause vasoconstriction and atrial natriuretic peptide promote vasodilation
accumulation of CO2, H, adenosine and low O2 cause vasodilation to increase perfusion