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

Control of Blood Flow- Exam 1 Flashcards

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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
What can flow get up to in reactive hyperemia?
Flow can increase 4-7x normal
26
Local control mechanisms are only functional as long as _______ doesn't change.
MAP
27
What will be affected if MAP changes?
All tissue will be affected by a change in flow; all tissues would see some type of local control response
28
What are the two theories relating to ability to keep flow through tissue close to normal over autoregulatory range?
Myogenic theory | metabolic theory
29
Myogenic Theory
Sudden stretch of small blood vessels cause surrounding smooth muscle of vessel wall to contract
30
According to the myogenic theory, what does increased blood pressure result in?
Stretches small blood vessels triggering reactive constriction thus reducing blood flow
31
According to the myogenic theory, what does decreased blood pressure result in?
Decreased stretch of small blood vessels triggering reactive relaxation and increased blood flow
32
According to the myogenic theory, what changes are vessels responding to?
Changes in pressure, not changes in flow
33
Endothelial-Derived Control Factors
Release several substances that interact directly with the smooth muscle to cause relaxation or constriction Ex. Nitric Oxide and endothelin
34
Nitric oxide
Importnat direct vasodilator; lipophilic gas
35
Endothelin
potent vasconstrictor; large amino acid peptide
36
What causes nitric oxide to be released?
Chemicals: Calcium & Angiotensin II | Physical stimuli: Shear stress due to increased flow
37
Where does nitric oxide mainly act?
Larger vessels upstream of metarterioles and precapillary sphincters
38
What happens when flow through capillary increases release of NO?
Causes corresponding dilation of the larger upstream vessels
39
What is a consequence of chronic hypertension or atherosclerosis?
Decreased NO release
40
What is the 1/2 life of NO?
6 seconds, moves into smooth muscle quickly
41
How is NO formed?
Arginine + Oxygen in the presence of nitric oxide synthase (NOS)
42
What does NO activate?
Soluble guanylate cyclase (SGC)
43
What does guanylate cyclase do?
Mediates conversion of cyclic guanosine triphosphate (cGTP) to cyclic guanosine monophosphate (cGMP)
44
What does cGMP activate?
cGMP-dependent protein kinase (PKG)
45
What does PKG ultimately lead to?
Relaxation of the smooth muscles
46
Where is endothelin present?
In all endothelial cells but concentration increases with vessel injury
47
Where is endothelin released?
Damaged cells
48
Endothelin can close arterial vessels as large as what diameter?
5mm
49
What happens if your pressure increases 100 to 150 mmHg (no change in metabolism)?
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
What would happen if you had a permanent increase in blood pressure?
Flow would slowly decrease over the next few weeks until flow back to original value
51
Short term changes in MAP attenuate changes in flow over what pressure range?
75 to 175 mmHg
52
Long-term changes able to keep flow normal over pressure range of what?
50 to 250 mmHg
53
Angiogenesis
increase in vascularity
54
Chronic increase in tissue metabolism/ chronic decrease in pressure produces what?
Angiogenesis
55
What changes as part of long term control?
Total number of arterioles and capillaries would increase | Size of existing arterioles and capillaries would increase
56
How long does it take for long-term vascularity changes to occur?
Days in younger patients | Weeks to months in older patients
57
What does the total change in vascularity depend on?
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
What are vascular endothelial growth factors
Small peptides that promote new vessel growth from existing vessels
59
What are some examples of endothelial growth factors?
Vascular endothelial growth factor (VEGF) Fibroblast growth factor Angiogenin
60
What are antiangiogenic substances?
Block the growth of new vessels Ex. angiostatin, endostatin potential anticancer agent
61
How do antiangiogenic substances act as anticancer agents?
cancer cells cannot grow into tumors unless they are able to develop an adequate blood supply, so they block the blood supply
62
Vasoconstrictor agnets
norepinephrine epinephrine angiotensin ii vasopressin
63
Norepinephrine
potent constrictor, released via ANS and adrenal medullae
64
Epinphrine
vasoconstrictor, not as potent as norepi
65
Angiotensin II
vasoconstrictor; part of the overall regulation of blood pressure
66
How many grams of Angiotensin II can increase arterial pressure 50 mmHg?
1/1,000,000 gram
67
Vasopressin
ADH | More powerful than angiotensin ii
68
Where is vasopressin released?
posterior pituitary
69
What is the major role of vasopressin?
increase water reabsorption by the kidneys
70
What is the vasopressin role during acute hypovolemia?
Vasoactive role
71
What are the vasodilator agents?
Bradykinin | Histamine
72
What are kinins?
Small peptides split from alpha2-globulins by proteolytic enzymes
73
Kallikrein
proteolytic enzyme in the blood (inactive)
74
how is kallikrein activated?
damage to blood, inflammation
75
What does activated kallikrein interact with?
Alpha2-globulin to release kallidin
76
What is kallidin converted to?
Converted by tissue enzymes to bradykinin
77
Bradykinin
causes powerful vasodilation and increased capillary permeability; important responses during inflammation
78
Histamine is released by what?
Mast cells and basophils located in damaged or inflamed tissue
79
What is histamine?
potent vasodilator and increases capillary permeability; can result in edema, allergic rxns
80
What are some ions that act on smooth muscle?
``` Calcium potassium magnesium hydrogen acetate/citrate ```
81
Calcium
increased levels stimulate smooth muscle contraction leading to vasoconstriction
82
Potassium
increased levels inhibit smooth muscle contraction leading to vasodilation
83
Magnesium
increased levels cause significnat vasodilation by inhibiting smooth muscle contraction
84
How are potassium and magnesium acting?
Changing resting membrane potentials
85
Hydrogen
increased levels result in vasodilation; a slight decrease in hydrogen ions cause arterioles constriction
86
Acetate/citrate
increased levels cause mild vasodilation

Physio II (14 decks)

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