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Cardiovascular System Module > Lecture 13 > Flashcards

Lecture 13 Flashcards

1
Q

What is blood flow like in all tissues?

A

Enormous variation in blood flow possible within tissues (e.g. resting versus active muscle)

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2
Q

What tissue has the most blood flow at rest?

A

The kidneys

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3
Q

What tissue has the most blood flow at maximum?

A

Salivary glands

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4
Q

What determines flow in a vessel?

A

Poiseuilles law - resistance to steady laminar flow

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5
Q

What is the main determinant of flow?

A

Radius

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6
Q

What are the two types of vascular control?

A

Intrinsic and extrinsic control

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7
Q

What does intrinsic mean?

A

Within the vascular wall

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8
Q

What is intrinsic control?

A

Blood vessels automatically adjust their own vascular tone by dilating or constricting in response to change of environment

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9
Q

What is extrinsic control?

A

Includes, neuronal, humoral, reflex and chemical regulatory mechanisms . These regulate the heart and myocardial contractility, and vascular smooth muscle to maintain cardiac output

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10
Q

What does local control adjust?

A

Blood flow in a tissue, independent of neural and hormonal effects

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11
Q

What does local control do?

A

Ensures matching of blood supply with needs of tissue and regulates capillary filtration pressure

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12
Q

What is metabolic hyperaemia?

A

Flow in most tissues is proportional to metabolic rate of tissue

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13
Q

What is reactive hyperaemia?

A

Increased flow following occlusion response to ischaemia (post-Ischaemic)

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14
Q

What is autoregulation?

A

Keeps flow constant despite changes in perfusion pressure

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15
Q

What is hyperaemia?

A

Increase in blood flow

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16
Q

What happens in heart muscle, skeletal muscle and brain tissue?

A

Blood flow increases steeply with increased metabolic rate

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17
Q

What do metabolic vasodilators do?

A

Act locally on resistance vessels

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18
Q

What is a way to increase blood flow?

A

Increase vasodilation

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19
Q

What is adenosine?

A

A byproduct and breakdown of ATP

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20
Q

What mediates metabolic hyperaemia?

A

Adenosine and interstitial K+

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21
Q

What contains adenosine?

A

Lots of vascular tissue have adenosine receptors particularly found in skeletal muscles and myocardium

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22
Q

How do you get adenosine?

A

Increase in metabolism, breakdown of ATP to ADP and AMP, AMP breaks down into adenosine

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23
Q

What do muscle cell proteins produce (GS proteins)?

A

Adenosine 2A

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24
Q

What is the mechanism for adenosine 2A produced from muscle cell Gs proteins?

A

Causes a decrease in phosphorylation which causes relaxation and vasodilation and also decreases sensitivity to ca2+

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25
Q

What are A1 receptors coupled to?

A

Coupled to K+ ATP channels and this causes hyperpolarisation which causes vasodilation

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26
Q

When is interstitial K+ activated?

A

During skeletal muscle contraction of neural activity

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27
Q

What is the mechanism for interstitial K+?

A

Increase in firing builds up K+ outside of cell during repolarisation which causes hyperpolarisation of muscle cells which leads to vasodilation

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28
Q

What else mediates metabolic hyperaemia?

A

Acidosis and hypoxia

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29
Q

What are cerebral blood vessels sensitive to?

A

Changes in CO2

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30
Q

What are the mechanisms for acidosis?

A

Hyperpolarisation of smooth muscle cell membrane reducing open probability of ca2+ channels.
nitric oxide release from endothelial cells.
Cerebral blood vessels sensitive to PCO2.
Skeletal muscle and myocardium insensitive.

31
Q

How does acidosis cause vasodilation?

A

Increase in metabolism, increase in PCO2 and lactic acid = vasodilation

32
Q

How does hypoxia cause vasodilation?

A

Increase in metabolism, decreases PO2 causes vasodilation

33
Q

What are cerebral blood vessels, skeletal muscle and myocardium sensitive to?

A

Hypoxia

34
Q

What happens in a pulmonary vasculature?

A

Decrease in PO2 leads to vasoconstriction (hypoxia pulmonary vasoconstriction)

35
Q

What does hypoxia and a build up of metabolites (PCO2, adenosine and Latic acid) generate?

A

Vasodilation and high flow when occlusion is removed

36
Q

What is reactive hyperaemia?

A

Transient increase in organ blood flow after a period of occlusion/ ischaemia

37
Q

What is increase in flow proportional to in reactive hyperaemia?

A

Duration of occlusion

38
Q

What is magnitude and duration of increase flow dependent on?

A

Length of time of occlusion

39
Q

What happens if you block off the flow to the tissue?

A

The tissue will become hypoxic and metabolic factors for hyperaemia are introduced, as the flow goes through the factors, they are washed away and acidosis and hypoxia disappears - blood flow returns to normal

40
Q

What is auto regulation of blood flow?

A

Keeps the blood flow relatively steady

41
Q

What does an increase in perfusion of pressure initially generate?

A

An increase in blood flow, followed by a rapid decrease in blood flow, towards control levels

42
Q

Where does auto regulation occur?

A

In many vascular beds, a rapid response of constriction will prevent damage

43
Q

What is the protective effect?

A

Autoregulation keeps flow almost constant within physiological pressure ranges

44
Q

Who first described the myogenic response?

A

William baylis in 1902

45
Q

What is a pressurised artery?

A

As long as the pressure is elevated the blood vessel will stay contracted

46
Q

What is the myogenic response?

A

When there is increased internal pressure blood vessels contract, when there is decrease in pressure blood vessels dilate

47
Q

What does the myogenic response do?

A

Managing flow in the vessel while an increase in pressure

48
Q

What is an increase in pressure associated with?

A

A rapid decrease in vessel diameter

49
Q

Why is the myogenic response a quick process?

A

So it will protect the downstream blood vessels

50
Q

What is the myogenic response independent of?

A

It is independent of the endothelium and of endothelial derived signalling

51
Q

What happens to the myocytes when there is an increase in pressure?

A

There is an initial stretch in the myocytes

52
Q

What does an increase in stretch in the myocytes cause?

A

Opens the TRP non selective cation channels, Cl- channels and ENACs

53
Q

How does ca2+ help with contraction in the myogenic response?

A

Depolarisation of smooth muscle cells increases ca2+ influx through L type calcium channels and causes contraction

54
Q

What is the ca2+ role in the myogenic response impaired by?

A

Ca2+ channel blockers, gandolinium, Cl- channel blockers and amiloride

55
Q

What are other mechanisms that could be involved in the myogenic response?

A

Proposer mechanosensors, calcium sensitisation pathways, depolarisation by 20-HETE

56
Q

What is 20-HETE?

A

It is a vasoconstrictor derived from arachidonic acid which reduces KCa

57
Q

What are some proposed mechanosensors?

A

Vascular smooth muscle cell-extracellular matrix adhesion through integrins, cell-cell adhesion through Cadherins, cytoskeleton components and membrane bound components

58
Q

What can change in autoregulation?

A

You can change the set point, the presence of metabolic hyperaemia can shift the steady steady of blood flow to a high level

59
Q

What does histamine do?

A

It is a inflammatory mediator, increases local blood flow and increases fluid movement into tissue

60
Q

What are the two different types of histamine receptors?

A

H1 and H2

61
Q

What does H1 receptor do in blood flow?

A

Increases vasoconstriction of venules and permeability of venules and capillaries

62
Q

What does the H2 receptor do in blood flow?

A

Increases vasodilation in arterioles

63
Q

What does serotonin do (5HT)?

A

Acts to increase vasoconstriction and permeability of venules and capillaries

64
Q

Where is serotonin found?

A

Endothelium, platelets and central nervous system

65
Q

What is thromboxane?

A

A vasoconstrictor and thrombotic agent released by platelets and endothelium

66
Q

What does aspirin do?

A

It can inhibit COX platelets, providing protection against thrombosis

67
Q

What are prostaglandins synthesised by?

A

Endothelium, fibroblasts, macrophages and leukocytes

68
Q

What are PGFs?

A

Vasoconstrictor

69
Q

What are PGEs and PGIs?

A

Vasodilators

70
Q

What is another vasodilator?

A

Bradykinin

71
Q

What is a vasoconstrictor?

A

Platelet activating factor

72
Q

What is the hierarchy of vascular control?

A

Autoregulation of intrinsic myogenic response,
Intrinsic modulators of autoregulated flow,
Extrinsic factors that override intrinsic controls to meet the demands of the whole body

73
Q

What are examples of intrinsic modulators?

A

Endothelial derived factors, metabolic and autacoids

Cardiovascular System Module (18 decks)

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