Control of Blood Vessels: Blood Flow Regulation Flashcards
Cerebral cardiac output
14% at rest
Factors that may regulate blood flow in different vascular beds
neural hormones local mechanical special features
Neural control of cerebral blood flow
relatively minor (α vasoconstriction)
Hormonal control of cerebral blood flow
minor
Local control of cerebral blood flow
autoregulation over wide range of pressure
important metabolic control during mental activity (regional). H+, K+, adenosine, hypercapnia, hypoxia -vasodilatation
Endothelin may be important vasoconstrictor in pathological states e.g. subarachnoid haemorrhage
Mechanical control of cerebral blood flow
constrained in rigid cranium; importantly influenced by CSF pressure e.g., space-occupying lesions increase ICP & reduce CBF
Special features that control cerebral blood flow
medullary ischaemic reflex (Cushing) e.g., tumour-induced reduction in CBF causes medullary ischaemia which stimulates an increase in BP in an attempt to restore CBF
Cardiac output for coronary
4%
Neural control of coronary blood flow
minor direct influence (α vasoconstriction) but secondary effect on flow due to changes in cardiac function and hence metabolism
Sympathetic stimulation causes b-mediated increase in HR & StV which increases O2 consumption
Local control of coronary blood flow
major influence of metabolites: hypoxia, hypercapnia, adenosine cause vasodilatation
Hormonal control of coronary blood flow
adrenaline - vasodilator and stimulates metabolism
Mechanical control of coronary blood flow
major influence on flow during the cardiac cycle;
peak flow in early diastole, zero or negative flow at onset of systole
compression at systole and relief of compression leads to increase of blood flow in diastole
Special feature control of coronary blood flow
parallelism between metabolism and flow
Skin cardiac output
4% at rest in thermoneutral environment
Neural control of skin blood flow
arterioles have a relatively weak innervation (α vasoconstriction)
A-V anastomoses have a dense innervation (α vasoconstriction)
increase in core temperature causes AVAs to dilate, increasing skin blood flow and hence heat loss
What do A-V anastomoses do?
capacity to deliver blood to the surface of the skin
Local control of skin blood flow
arterioles have some degree of myogenic autoregulation
A-V anastomoses show no autoregulation and no reactive hyperaemia
Endothelin may be involved in pathological states (Raynauds)
What is Raynauds?
resitriction of blood flow in digits
affects women more than men
Hormonal control of skin blood flow
angiotensin, vasopressin, noradrenaline, adrenaline all cause vasoconstriction
Mechanical control of skin blood flow
minimal
Special features control of skin blood flow
primary function is thermoregulation
sweat glands have sympathetic cholinergic innervation (sudomotor) - vasodilatation via release of e.g. bradykinin - leaky capillaries, vasodilatation in arterioles
Skeletal muscle cardiac output
15% at rest
Neural control of skeletal muscle blood flow
rest : important α vasoconstriction, some β vasodilatation, maybe sympathetic cholinergic vasodilatation
exercise: very little neural influence, some β vasodilatation
What is skeletal muscle involved in?
systemic BP regulation. Skeletal muscle ~ 40% of body mass, hence vasoconstriction has large influence on TPR
Local control of skeletal muscle blood flow
rest: neural control (baroreflexes) over-ride autoregulatory mechanisms
exercise: local metabolites have a major influence (K+, adenosine, lactate etc)
Hormonal control of skeletal muscle blood flow
adrenaline at low concentrations will vasodilate (β)
Mechanical control of skeletal muscle blood flow
muscle pumping
Special feature control of skeletal muscle blood flow
capacity to increase flow in exercise (20-fold) - active hyperaemia. Large increase in flow post-occlusion - reactive hyperaemia (increased blood flow)
Splanchnic cardiac output
superior mesenteric - 10%
hepatic - 25%
Neural control of splanchnic blood flow
intestinal: moderate α vasoconstriction,
hepatic: important α venoconstriction
Local control of splanchnic blood flow
intestinal: poor autoregulation but importantly influenced by local peptides, hepatic: portal vein - no autoregulation, hepatic artery - good autoregulation
Hormonal control of splanchnic blood flow
G-I hormones (gastrin, cholecystokinin) vasodilate; vasopressin, angiotensin constrict potently
Why is hepatic venoconstriction important?
liver stores around 15% of blood volume
hepatic venoconstriction can expel around 50% hepatic blood volume into circulation
Mechanical control of splanchnic blood flow
minimal
Special feature control of splanchnic blood flow
intestinal circulation exhibits functional hyperaemia following feeding
How is vasoconstriction in splanchnic vessels beneficial and detrimental?
+ baroreflex
- haemorrhage/septic shock
- intense vasoconstriction can lead to damage and release of toxins
Renal cardiac output
25%
Neural control of renal blood flow
important α vasoconstriction; some β vasodilatation
Renin secreting cells have a sympathetic innervation (β adrenoceptors)
Local control of renal blood flow
good autoregulation of flow over wide pressure range
Hormonal control of renal blood flow
noradrenaline, adrenaline, angiotensin can cause constriction vasopressin may cause vasodilatation via prostaglandin/NO release
dopamine causes vasodilatation
Mechanical control of renal blood flow
renal capsule may restrict flow due to compression of blood vessels in pathological states
Special feature of renal blood flow
excretory function of the kidney depends on well-maintained flow (autoregulation) vascular connections provide for capacity to regulate afferent/efferent resistances
Pulmonary cardiac output
100%
Neural control of pulmonary blood flow
relatively minor influence
α vasoconstriction
Local control of pulmonary blood flow
hypoxia causes vasoconstriction which is augmented by hypercapnia - possibly mediated by endothelin
NO causes dilatation - may be used therapeutically
Possible therapeutic strategies for pulmonary hypertension
endothelin receptor antagonism
NO inhalation
Mechanical control of pulmonary blood flow
flow 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
If alveolar pressure is > intravascular pressure, what does this mean?
flow is reduced
How does lung inflation affect resistance?
reduces resistance in extra-alveolar vessels (traction)
increases resistance in intra-alveolar vessels (compression)
Special feature control of pulmonary blood flow
thin walled vessels with low resistance and low vasoconstrictor capacity
hydrostatic pressure < colloid osmotic pressure - favours reabsorption
Why is a low hydrostatic pressure wanted and higher colloid?
so no fluid goes to the alveoli, preventing gas exchange
