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Circulation
Neural
Hormones
Local
Mechanical
Special Features
Cerebral
:
14% of Cardiac
Output
50ml/ 100g/min
Minor
-some alpha vasoconstriction
Minor influence
-
Good autoregulation over 60
-
160mmHg abolished by hypercapnia.
-H+, K+, hypercapnia, hypoxia and
adenosine cause vasodilatation
- Endothelin important vasoconstrictor
in pathological states- e.g. subarachnoid
haemorrhage
Constrained in rigid
cranium, influenced by CSF.
A space occupying lesion
will reduce cerebral blood
flow and increase intra
cranial pressure

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-
Medullary ischaemic reflex
(Cushing): A tumour induced
decrease in CBF causes
medullary ischaemia and
increases BP to restore CBF
Coronary:
4% Cardiac
output
~70ml/100g/min
Minor direct influence (a
-
vasoconstriction), but
secondary flow due to changes
in cardiac function and hence
metabolism.
-Sympathetic stimulation causes
B-mediated increase in StV and
HR which increases O2
consumption
Adrenaline is a
vasodilator and
stimulates
metabolism
Major influence of metabolites:
-hypoxia, hypercapnia, adenosine cause
vasodilatation
Major influence on flow
during cardiac cycle: peak

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flow in early diastole, zero

or negative flow at onset of
systole
Parallelism between
metabolism and flow.
(greater metabolism, greater
flow)
Skin:
4% of cardiac
output at rest in
thermoneutral
environment
1-200ml/
100g/min
A
-
V Anastomoses have a
denseinnervation (a-
vasoconstriction).
-Increase in core temperature
causes AVAs to dilate,
increasing skin blood flow and
hence heat loss
Angiotensin,
vasopressing,
noradrenaline and
adrenaline all
cause
vasoconstriction

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Arterioles show some degree of

myogenic autoregulation.
A-V anastomoses show no
autoregulation and no reactive
hyperaemia.
Endothelin may be involved in Raynauds
Minimal influence
Main function is
thermoregulation. Sweat
glands have sympathetic
cholinergic innervation
(sudomotor) which can cause
vasodilatation via release of
bradykinin
Skeletal muscle:
15% Cardiac
output at rest
3-60ml/100g
/min
-
At rest, important
vasoconstriction, some B-
vasodilatation, maybe some
sympathetic cholinergic
vasodilatation
-Involved in systemic BP
regulation. SkM~ 40% body
mass, hence vasoconstriction
has a large influence on TPR

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-Exercise: little neural influence,

some B-vasodilatation
Adrenaline at low
concentrations will
vasodilate (B-
mediated)
-
Rest: neural control (baroreflexes)
override autoregulatory mechanisms
-Exercise: local metabolites have a
major influence (K+, adenosine, lactate
etc.)
Muscle pumping
Capacity to increase flow in
exercise 20 fold- this is active
hyperaemia.
-Large increase in flow post-
occlusion- reactive
hyperaemia

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