Microcirculation Flashcards
INTRO
vessel structures and functions
artery
oxygenated blood
thick muscular wall to withstand high pressure
smaller lumen than veins
INTRO
vessel structures and functions
arteriole
oxygenated
thick, muscular wall to withstand high pressure and contract
RESISTANCE VESSEL
small lumen
INTRO
vessel structures and functions
capillary
where exchange occurs of gases and nutrients/waste metabolites
one cell thick wall = no muscle
low pressure
tiny lumen
INTRO
vessel structures and functions
venue
deoxygenated blood
low pressure
thin wall
compliant
INTRO
vessel structures and functions
veins
deoxygenated
low pressure like venue = valves prevent back flow and skeletal muscle aids pumping especially when stood upright
large lumen = CAPACITANCE VESSELS
compliant
INTRO
vessel structures and functions
what does microcirculation comprise of?
microcirculation = arterioles, met-arterioles, venues and capillaries
(although no control of microcirculation occurs at capillaries)
MODULATORS OF VASCULAR TONE
what is vascular tone (not sure ab this)
the degree of constriction experienced by a blood vessel in response to the resistance the blood has to overcome
high tone = more contraction = more vasoconstriction due to high resistance
low tone = less contraction = more vasodilation due to low resistance
MODULATION OF VASCULAR TONE
how can we modulate vascular tone?
extrinsic
- hormones
- neural
intrinsic
- vasoconstrictor and vasodilator chemicals
MODULATION OF VASCULAR TONE
how does the sympathetic nervous system extrinsically modulate tone?
- NA acts on A1 adrenoreceptors of smooth muscle
ATP is a co-transmitter that prolonged its vasoconstriction effects - A acts on B2 on arteries supplying skeletal muscle
= overall sympathetic effect is more towards skeletal muscles than internal organs
MODULATION OF VASCULAR TONE
what are the local vasoconstrictors?
- endothelins (ET-1 is most abundant) acting on ETa and ETb receptors of smooth muscle
- thromboxane in response to injury and thus platelet activation
MODULATION OF VASCULAR TONE
what are local vasodilators?
- Adenosine from ATP breakdown on A2 receptors
- NO from the endothelium when Ca2+ release is stimulated which binds to calmodulin to stimulate NO from endothelium
- prostacyclin from arachidonic acid metabolism
MODULATION OF VASCULAR TONE
how do vasoconstrictors and vasodilators work
dilators are opposite:
constrictors increase ca2+ in cytoplasm by opening stores in sarcoplasmic reticulum and opening voltage gates channels
calcium bind to calmodulin to stimulate MLCK
MLCK phosphorylates myosin so it can interact with actin
MECHANISM OF CONTROL
why does tone have to be regulated
tone is regulated to match metabolic needs
MECHANISM OF CONTROL
what 2 theories are there for the mechanism as to how blood flow increases to tissues that have an increased metabolic rate/low oxygen
vasodilatory theory
oxygen demand theory
MECHANISM OF CONTROL
explain the vasodilatory theory
less oxygen stimulates formation of vasodilator substances like adenosine and NO
e.g. in heart
when heart becomes more metabolically active and oxygen demand increases, this stimulates breakdown of ATP
adenosine then leaks out to cause coronary vasodilation
MECHANISM OF CONTROL
explain the oxygen demand theory
oxygen is needed to cause contraction
when there’s not enough, blood vessels relax and thus dilate
MECHANISM OF CONTROL
what is reactive hyperaemia?
when blood flow increases much more than normal following a blockage to blood supply = can last for hours depending on how long the blockage was
this is to repay the oxygen debt
MECHANISM OF CONTROL
what is active hyperaemia?
the increase in blood flow when tissue becomes highly active
increase metabolism means nutrients are used up and vasodilators are released rapidly = blood flow increases 20 fold
MECHANISM OF CONTROL
what is the extrinsic mechanism in skin?
anterior hypothalamus detect temperature
high temp = sympathetic system decreased to cause vasodilation= heat is lost
low temp = sympathetic innervation increased = vasoconstriction = retain heat
MECHANISM OF CONTROL
what is the local mechanism in skin?
increased temp reduces affinity of alpha 2 Receptors for NA
= less sympathetic effect
= less vasoconstriction
= vasodilation
CLINICAL
what is Raynaud’s phenomenon?
when low temp causes excessive vasoconstriction that blood flow is reduced
discolouration, skin atrophy, ulcers
caused by hyperactive sympathetic system = use vasodilators or inhibit sympathetic system
MECHANISM OF CONTROL
what is the difference with non-apical skin
in non-apical skin, sympathetic innervation causes vasodilation instead of vasoconstriction as EACh released instead of NA
HAEMODYNAMICS
what monitors blood pressure
baroreceptors in the aortic arch, pulmonary artery and carotid arteries monitor high blood pressure
baroreceptors in the atria and large veins monitor lower blood pressure
HAEMODYNAMICS
how do baroreceptors work
baroreceptor sends signal to upper medulla
medulla responds with sympathetic or parasympathetic response (whichever is appropriate)
HAEMODYNAMICS
explain the factors contributing to blood pressure
BP = blood flow x resistance
blood vol = increase vol increases pressure as closed system
compliancy = reduces pressure as resistance decreases (BP increases with age as compliance reduces)
HAEMODYNAMICS
what is cardiac output
blood leaving heart per unit time (usually per minute)
CO = stroke vol x heart rate
5L/min
HAEMODYNAMICS
what is the postural control reflex response
- stand up
- blood pools in legs and so preload of heart goes down
- thus cardiac output goes down which decreases blood vol and thus pressure
- baroreceptors detect and sympathetic system is triggered to vasoconstrict and increase heart rate
- vasoconstriction increases preload and thus stroke vol, heart rate increases thus cardiac output increases
- sympathetic system also causes vascular resistance to increase which forces an increases blood pressure so flow is constant
AUTOREGULATION
what is auto regulation?
when blood flow is maintained constant through negative feedback when there is a change in pressure that initially changes the flow
AUTOREGULATION
what are the 2 auto regulation theories?
- metabolic = pressure increases and washes out vasodilators = constriction = normal flow
- myogenic = high pressure stretches vessels which causes reactive constriction
= rapid entry of ca2+ from ECF into arteriole cells by stretch-induced vascular depolarisation
in low pressure the stretch is less so cells are polarised and no ca2+ enters = relaxation reduces vascular resistance and flow returns
AUTOREGULATION
which mechanism overbids the other?
metabolic factors override myogenic mechanism when metabolic demands increase significantly
EXPERIMENTAL
explain the experiment by McCarron and Crichton
- measures diameter of rat artery with changes in blood pressure
- increased then shortly decreased
- ca2+ influx caused constriction when the vessel stretched
