This document summarizes the circulation and key features of several vascular beds in the body. It discusses: 1. The cerebral circulation receives 14% of cardiac output and has good autoregulation over a wide range of blood pressures. Local factors like H+, K+, and adenosine cause vasodilation while endothelin causes vasoconstriction in pathological states. 2. The coronary circulation receives 4% of cardiac output. Flow parallels metabolism with greater metabolism resulting in greater flow. Local metabolites are a major influence on flow. 3. The skin circulation receives 4% of cardiac output at rest and is mainly involved in thermoregulation. Vasoconstrictors and vasodilators influence flow

1. 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
-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
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
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
-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

2. Splanchnic:
-Superior
mesentetic 10%
CO,
-hepatic 25% CO
(75% is via HPV,
25% via hepatic
artery)
Intestinal: moderate a-
vasoconstriction
-hepatic: important a
VENOconstriction
-Liver stores ~15% of blood
volume, hepatic
venoconstriction can expel 50%
hepatic blood volume into the
circulation
Gastrointestinal
hormones
(gastrinc,
cholecystokinin)
vasodilate
-vasopressin,
angiotensin
constrict
Intestinal@ poor autoregulation but
importantly influenced by local
peptides,
-hepatic portal vein- no autoregulation,
-hepatic artery: good autoregulation
Minimal influence Intestinal circulation exhibits
functional hyperaemia
following feeding.
Vasoconstriction can lead to
damage
-vasoconstriction
(neurohumoral) beneficial in
baroreflex but can be
detrimental in haemorrhage
or septic shock
Renal: 25%
Cardiac output
Important a-vasoconstriction,
some b-vasodilatation.
-Renin secreting cells have a
sympathetic innervation (b-
adrenoceptors)
NA, A, angiotensin
can cause
constriction
-Angiotensin and
vasopressin may
cause
vasodilatation via
prostaglandin/ NO
release
-Dopamine causes
vasodilatation
Good autoregulation of flow over a wide
pressure range
Renal capsule may restrict
flow in pathological states
Excretory function of the
kidney depends on well-
maintained flow
(autoregulation). Vascular
connections provide for
capacity to regulate
afferent/efferent resistances
Pulmonary:
100% Cardiac
output
Relatively minor neural
influence (vasoconstriction)
Unlike elsewhere, hypoxia causes
vasoconstriction which is augmented by
hypercapnia- possibly mediated by
endothelin
-NO causes dilatation so can be used
therapeutically
-Pulmonary hypertension: use
endothelin receptor antagonists, and
NO inhalation.
Flow is affected by changes
in alveolar pressure and
lung volume. Increase in
flow (Cardiac output)
associated with recruitment
and distension of
microvessels and a
decrease in vascular
resistance
-Alveolar P > intravascular
P, flow is reduced
-Lung inflation reduces
resistance in extra-alveolar
vessels, increases resistance
in intra-alveolar vessels
Thin walled vessels with low
resistance, low
vasoconstrictor capacity.
Hydrostatic pressure < colloid
osmotic pressure, it favours
reabsorption
(Hydrostatic P ~10mmHg
Colloid osmotic P ~25mmHg)