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
Q

Local control of skeletal muscle blood flow

A

rest: neural control (baroreflexes) over-ride autoregulatory mechanisms
exercise: local metabolites have a major influence (K+, adenosine, lactate etc)

26
Q

Hormonal control of skeletal muscle blood flow

A

adrenaline at low concentrations will vasodilate (β)

27
Q

Mechanical control of skeletal muscle blood flow

A

muscle pumping

28
Q

Special feature control of skeletal muscle blood flow

A

capacity to increase flow in exercise (20-fold) - active hyperaemia. Large increase in flow post-occlusion - reactive hyperaemia (increased blood flow)

29
Q

Splanchnic cardiac output

A

superior mesenteric - 10%

hepatic - 25%

30
Q

Neural control of splanchnic blood flow

A

intestinal: moderate α vasoconstriction,
hepatic: important α venoconstriction

31
Q

Local control of splanchnic blood flow

A

intestinal: poor autoregulation but importantly influenced by local peptides, hepatic: portal vein - no autoregulation, hepatic artery - good autoregulation

32
Q

Hormonal control of splanchnic blood flow

A

G-I hormones (gastrin, cholecystokinin) vasodilate; vasopressin, angiotensin constrict potently

33
Q

Why is hepatic venoconstriction important?

A

liver stores around 15% of blood volume

hepatic venoconstriction can expel around 50% hepatic blood volume into circulation

34
Q

Mechanical control of splanchnic blood flow

A

minimal

35
Q

Special feature control of splanchnic blood flow

A

intestinal circulation exhibits functional hyperaemia following feeding

36
Q

How is vasoconstriction in splanchnic vessels beneficial and detrimental?

A

+ baroreflex

  • haemorrhage/septic shock
  • intense vasoconstriction can lead to damage and release of toxins
37
Q

Renal cardiac output

A

25%

38
Q

Neural control of renal blood flow

A

important α vasoconstriction; some β vasodilatation

Renin secreting cells have a sympathetic innervation (β adrenoceptors)

39
Q

Local control of renal blood flow

A

good autoregulation of flow over wide pressure range

40
Q

Hormonal control of renal blood flow

A

noradrenaline, adrenaline, angiotensin can cause constriction vasopressin may cause vasodilatation via prostaglandin/NO release
dopamine causes vasodilatation

41
Q

Mechanical control of renal blood flow

A

renal capsule may restrict flow due to compression of blood vessels in pathological states

42
Q

Special feature of renal blood flow

A

excretory function of the kidney depends on well-maintained flow (autoregulation) vascular connections provide for capacity to regulate afferent/efferent resistances

43
Q

Pulmonary cardiac output

A

100%

44
Q

Neural control of pulmonary blood flow

A

relatively minor influence

α vasoconstriction

45
Q

Local control of pulmonary blood flow

A

hypoxia causes vasoconstriction which is augmented by hypercapnia - possibly mediated by endothelin
NO causes dilatation - may be used therapeutically

46
Q

Possible therapeutic strategies for pulmonary hypertension

A

endothelin receptor antagonism

NO inhalation

47
Q

Mechanical control of pulmonary blood flow

A

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
Q

If alveolar pressure is > intravascular pressure, what does this mean?

A

flow is reduced

49
Q

How does lung inflation affect resistance?

A

reduces resistance in extra-alveolar vessels (traction)

increases resistance in intra-alveolar vessels (compression)

50
Q

Special feature control of pulmonary blood flow

A

thin walled vessels with low resistance and low vasoconstrictor capacity
hydrostatic pressure < colloid osmotic pressure - favours reabsorption

51
Q

Why is a low hydrostatic pressure wanted and higher colloid?

A

so no fluid goes to the alveoli, preventing gas exchange