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Physio II > Control of Blood Flow- Exam 1 > Flashcards

Control of Blood Flow- Exam 1 Flashcards

1
Q

What are the 4 components of maintaining tissue demand?

A

Delivery of oxygen and other nutrients
Removal of waste (co2 and hydrogen ions)
Maintain appropriate ion concentrations
Supply needed hormones

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2
Q

How is acute (metabolic control) response controlled?

A

Vasodilation/vasoconstriction of arterioles, metarterioles, precapillary sphincters

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3
Q

How is long term response controlled?

A

Increasing/decreasing physical size and number of blood vessels within tissue

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4
Q

Which type of response is finite?

A

Acute (metabolic control)

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5
Q

Which type of response is infinite?

A

Long-term response

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6
Q

How long does it take for an acute (metabolic) response to occur?

A

Response occurs within seconds (sudden change in metabolism; oxygen content; input pressure)

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7
Q

How long does it take for a long-term response to occur?

A

Takes days/weeks (more permanent changes in metabolism; oxygen content, input pressure)

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8
Q

An 8-fold increase in metabolism results in what increase in blood flow through tissue?

A

4-fold increase in blood flow

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9
Q

What are 4 examples of decrease in arterial oxygen sat resulting in increased blood flow?

A
  1. High altitude
  2. Pneumonia
  3. Carbon monoxide poisoning
  4. cyanide poisoning
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10
Q

What opens and closes multiple times each minute?

A

precapillary sphincters

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11
Q

What are the two theories for acute regulation?

A

Oxygen (nutrient) lack theory

Vasodilator theory

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12
Q

Oxygen (nutrient) lack theory

A

Oxygen & other nutrients needed for smooth muscle contraction
When nutrients not available - muscle relaxes/dilation
Metabolism increases local decrease in oxygen content results in vasodilation

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13
Q

Vasodilator Theory

A

Metabolism increases production/concentration of metabolic waste increases
Metabolic waste interacts with smooth muscle resulting in dilation

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14
Q

What do the theories for acute regulation affect?

A

Tone of smooth muscle mainly in metarterioles and precapillary sphincters with some affect on arterioles

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15
Q

What does the overall tone of arterioles depend on?

A

Tone of autonomic nervous system

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16
Q

What determines the overall concentration of vasodilator factors?

A

Equilibrium between metabolic rate and flow through tissue

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17
Q

Potential Vasoactive Substances

A 
Adenosine
Carbon dioxide
Adenosine phosphate compounds
Histamine
Potassium ions
Hydrogen ions
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18
Q

What releases adenosine?

A

Cardiac cells when coronary blood flow inadequate, oxygen concentration has decreased and stores of ATP has decreased

Tissue in response to decreased oxygen concentration

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19
Q

What is carbon dioxide and where is it most relevant?

A

Potent vasodilator especially in the brain

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20
Q

What do Adenosine Phosphate compounds result from?

A

Increased ATP degradation

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21
Q

What is histamine and where is it released?

A

Potent vasodilator released from mast cells and basophils

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22
Q

When are hydrogen ions released?

A

Released from tissue in form of lactic acid in response to decreased oxygen concentration

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23
Q

Active Hyperemia

A

Response to increased metabolic demand with a tissue

Ex. increased metabolic activity in skeletal muscle

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24
Q

Reactive Hyperemia

A

Response of tissue to no flow (ischemia)

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25
Q

What can flow get up to in reactive hyperemia?

A

Flow can increase 4-7x normal

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26
Q

Local control mechanisms are only functional as long as _______ doesn’t change.

A

MAP

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27
Q

What will be affected if MAP changes?

A

All tissue will be affected by a change in flow; all tissues would see some type of local control response

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28
Q

What are the two theories relating to ability to keep flow through tissue close to normal over autoregulatory range?

A

Myogenic theory

metabolic theory

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29
Q

Myogenic Theory

A

Sudden stretch of small blood vessels cause surrounding smooth muscle of vessel wall to contract

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30
Q

According to the myogenic theory, what does increased blood pressure result in?

A

Stretches small blood vessels triggering reactive constriction thus reducing blood flow

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31
Q

According to the myogenic theory, what does decreased blood pressure result in?

A

Decreased stretch of small blood vessels triggering reactive relaxation and increased blood flow

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32
Q

According to the myogenic theory, what changes are vessels responding to?

A

Changes in pressure, not changes in flow

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33
Q

Endothelial-Derived Control Factors

A

Release several substances that interact directly with the smooth muscle to cause relaxation or constriction

Ex. Nitric Oxide and endothelin

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34
Q

Nitric oxide

A

Importnat direct vasodilator; lipophilic gas

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35
Q

Endothelin

A

potent vasconstrictor; large amino acid peptide

36
Q

What causes nitric oxide to be released?

A

Chemicals: Calcium & Angiotensin II

Physical stimuli: Shear stress due to increased flow

37
Q

Where does nitric oxide mainly act?

A

Larger vessels upstream of metarterioles and precapillary sphincters

38
Q

What happens when flow through capillary increases release of NO?

A

Causes corresponding dilation of the larger upstream vessels

39
Q

What is a consequence of chronic hypertension or atherosclerosis?

A

Decreased NO release

40
Q

What is the 1/2 life of NO?

A

6 seconds, moves into smooth muscle quickly

41
Q

How is NO formed?

A

Arginine + Oxygen in the presence of nitric oxide synthase (NOS)

42
Q

What does NO activate?

A

Soluble guanylate cyclase (SGC)

43
Q

What does guanylate cyclase do?

A

Mediates conversion of cyclic guanosine triphosphate (cGTP) to cyclic guanosine monophosphate (cGMP)

44
Q

What does cGMP activate?

A

cGMP-dependent protein kinase (PKG)

45
Q

What does PKG ultimately lead to?

A

Relaxation of the smooth muscles

46
Q

Where is endothelin present?

A

In all endothelial cells but concentration increases with vessel injury

47
Q

Where is endothelin released?

A

Damaged cells

48
Q

Endothelin can close arterial vessels as large as what diameter?

A

5mm

49
Q

What happens if your pressure increases 100 to 150 mmHg (no change in metabolism)?

A

Quick increase in blood flow- 30 sec to 2 min
Local constriction, decrease in flow
When complete, flow still 10 to 15 % higher than needed

50
Q

What would happen if you had a permanent increase in blood pressure?

A

Flow would slowly decrease over the next few weeks until flow back to original value

51
Q

Short term changes in MAP attenuate changes in flow over what pressure range?

A

75 to 175 mmHg

52
Q

Long-term changes able to keep flow normal over pressure range of what?

A

50 to 250 mmHg

53
Q

Angiogenesis

A

increase in vascularity

54
Q

Chronic increase in tissue metabolism/ chronic decrease in pressure produces what?

A

Angiogenesis

55
Q

What changes as part of long term control?

A

Total number of arterioles and capillaries would increase

Size of existing arterioles and capillaries would increase

56
Q

How long does it take for long-term vascularity changes to occur?

A

Days in younger patients

Weeks to months in older patients

57
Q

What does the total change in vascularity depend on?

A

Maximum blood flow needed by tissue (allows tissue to response to exercise or other times when tissue flow has to increase to meet a short term need)

58
Q

What are vascular endothelial growth factors

A

Small peptides that promote new vessel growth from existing vessels

59
Q

What are some examples of endothelial growth factors?

A

Vascular endothelial growth factor (VEGF)
Fibroblast growth factor
Angiogenin

60
Q

What are antiangiogenic substances?

A

Block the growth of new vessels
Ex. angiostatin, endostatin

potential anticancer agent

61
Q

How do antiangiogenic substances act as anticancer agents?

A

cancer cells cannot grow into tumors unless they are able to develop an adequate blood supply, so they block the blood supply

62
Q

Vasoconstrictor agnets

A

norepinephrine
epinephrine
angiotensin ii
vasopressin

63
Q

Norepinephrine

A

potent constrictor, released via ANS and adrenal medullae

64
Q

Epinphrine

A

vasoconstrictor, not as potent as norepi

65
Q

Angiotensin II

A

vasoconstrictor; part of the overall regulation of blood pressure

66
Q

How many grams of Angiotensin II can increase arterial pressure 50 mmHg?

A

1/1,000,000 gram

67
Q

Vasopressin

A

ADH

More powerful than angiotensin ii

68
Q

Where is vasopressin released?

A

posterior pituitary

69
Q

What is the major role of vasopressin?

A

increase water reabsorption by the kidneys

70
Q

What is the vasopressin role during acute hypovolemia?

A

Vasoactive role

71
Q

What are the vasodilator agents?

A

Bradykinin

Histamine

72
Q

What are kinins?

A

Small peptides split from alpha2-globulins by proteolytic enzymes

73
Q

Kallikrein

A

proteolytic enzyme in the blood (inactive)

74
Q

how is kallikrein activated?

A

damage to blood, inflammation

75
Q

What does activated kallikrein interact with?

A

Alpha2-globulin to release kallidin

76
Q

What is kallidin converted to?

A

Converted by tissue enzymes to bradykinin

77
Q

Bradykinin

A

causes powerful vasodilation and increased capillary permeability; important responses during inflammation

78
Q

Histamine is released by what?

A

Mast cells and basophils located in damaged or inflamed tissue

79
Q

What is histamine?

A

potent vasodilator and increases capillary permeability; can result in edema, allergic rxns

80
Q

What are some ions that act on smooth muscle?

A 
Calcium 
potassium
magnesium
hydrogen
acetate/citrate
81
Q

Calcium

A

increased levels stimulate smooth muscle contraction leading to vasoconstriction

82
Q

Potassium

A

increased levels inhibit smooth muscle contraction leading to vasodilation

83
Q

Magnesium

A

increased levels cause significnat vasodilation by inhibiting smooth muscle contraction

84
Q

How are potassium and magnesium acting?

A

Changing resting membrane potentials

85
Q

Hydrogen

A

increased levels result in vasodilation; a slight decrease in hydrogen ions cause arterioles constriction

86
Q

Acetate/citrate

A

increased levels cause mild vasodilation

Physio II (14 decks)

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