Control of Blood Vessels: Blood Flow Regulation Flashcards

1
Q

Cerebral cardiac output

A

14% at rest

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2
Q

Factors that may regulate blood flow in different vascular beds

A
neural
hormones
local
mechanical
special features
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3
Q

Neural control of cerebral blood flow

A
relatively minor
(α vasoconstriction)
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4
Q

Hormonal control of cerebral blood flow

A

minor

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5
Q

Local control of cerebral blood flow

A

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

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6
Q

Mechanical control of cerebral blood flow

A

constrained in rigid cranium; importantly influenced by CSF pressure e.g., space-occupying lesions increase ICP & reduce CBF

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7
Q

Special features that control cerebral blood flow

A

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

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8
Q

Cardiac output for coronary

A

4%

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9
Q

Neural control of coronary blood flow

A

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

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10
Q

Local control of coronary blood flow

A

major influence of metabolites: hypoxia, hypercapnia, adenosine cause vasodilatation

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11
Q

Hormonal control of coronary blood flow

A

adrenaline - vasodilator and stimulates metabolism

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12
Q

Mechanical control of coronary blood flow

A

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

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13
Q

Special feature control of coronary blood flow

A

parallelism between metabolism and flow

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14
Q

Skin cardiac output

A

4% at rest in thermoneutral environment

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15
Q

Neural control of skin blood flow

A

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

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16
Q

What do A-V anastomoses do?

A

capacity to deliver blood to the surface of the skin

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17
Q

Local control of skin blood flow

A

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)

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18
Q

What is Raynauds?

A

resitriction of blood flow in digits

affects women more than men

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19
Q

Hormonal control of skin blood flow

A

angiotensin, vasopressin, noradrenaline, adrenaline all cause vasoconstriction

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20
Q

Mechanical control of skin blood flow

A

minimal

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21
Q

Special features control of skin blood flow

A

primary function is thermoregulation
sweat glands have sympathetic cholinergic innervation (sudomotor) - vasodilatation via release of e.g. bradykinin - leaky capillaries, vasodilatation in arterioles

22
Q

Skeletal muscle cardiac output

A

15% at rest

23
Q

Neural control of skeletal muscle blood flow

A

rest : important α vasoconstriction, some β vasodilatation, maybe sympathetic cholinergic vasodilatation
exercise: very little neural influence, some β vasodilatation

24
Q

What is skeletal muscle involved in?

A

systemic BP regulation. Skeletal muscle ~ 40% of body mass, hence vasoconstriction has large influence on TPR

25
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)
26
Hormonal control of skeletal muscle blood flow
adrenaline at low concentrations will vasodilate (β)
27
Mechanical control of skeletal muscle blood flow
muscle pumping
28
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)
29
Splanchnic cardiac output
superior mesenteric - 10% | hepatic - 25%
30
Neural control of splanchnic blood flow
intestinal: moderate α vasoconstriction, hepatic: important α venoconstriction
31
Local control of splanchnic blood flow
intestinal: poor autoregulation but importantly influenced by local peptides, hepatic: portal vein - no autoregulation, hepatic artery - good autoregulation
32
Hormonal control of splanchnic blood flow
G-I hormones (gastrin, cholecystokinin) vasodilate; vasopressin, angiotensin constrict potently
33
Why is hepatic venoconstriction important?
liver stores around 15% of blood volume | hepatic venoconstriction can expel around 50% hepatic blood volume into circulation
34
Mechanical control of splanchnic blood flow
minimal
35
Special feature control of splanchnic blood flow
intestinal circulation exhibits functional hyperaemia following feeding
36
How is vasoconstriction in splanchnic vessels beneficial and detrimental?
+ baroreflex - haemorrhage/septic shock - intense vasoconstriction can lead to damage and release of toxins
37
Renal cardiac output
25%
38
Neural control of renal blood flow
important α vasoconstriction; some β vasodilatation | Renin secreting cells have a sympathetic innervation (β adrenoceptors)
39
Local control of renal blood flow
good autoregulation of flow over wide pressure range
40
Hormonal control of renal blood flow
noradrenaline, adrenaline, angiotensin can cause constriction vasopressin may cause vasodilatation via prostaglandin/NO release dopamine causes vasodilatation
41
Mechanical control of renal blood flow
renal capsule may restrict flow due to compression of blood vessels in pathological states
42
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
43
Pulmonary cardiac output
100%
44
Neural control of pulmonary blood flow
relatively minor influence | α vasoconstriction
45
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
46
Possible therapeutic strategies for pulmonary hypertension
endothelin receptor antagonism | NO inhalation
47
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
48
If alveolar pressure is > intravascular pressure, what does this mean?
flow is reduced
49
How does lung inflation affect resistance?
reduces resistance in extra-alveolar vessels (traction) | increases resistance in intra-alveolar vessels (compression)
50
Special feature control of pulmonary blood flow
thin walled vessels with low resistance and low vasoconstrictor capacity hydrostatic pressure < colloid osmotic pressure - favours reabsorption
51
Why is a low hydrostatic pressure wanted and higher colloid?
so no fluid goes to the alveoli, preventing gas exchange