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Physiology > control of blood flow > Flashcards

control of blood flow Flashcards

1
Q

Acute (metabolic control)

A

response in seconds. finite response. Controlled mainly vasodilation / vasoconstriction of
arterioles, metarterioles, precapillary sphincters

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2
Q

 Long-term

A

sow response – takes days / weeks
 More permanent changes in metabolism; oxygen content; input
pressure
 Almost infinite response
 Controlled by increasing / decreasing physical size and
number of blood vessels within tissue

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3
Q

8 fold increase in metabolism results in

A

four fold increase in BF

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4
Q

Acute Control – Response to Decrease in oxygen

A 
results in an increase in blood flow through the tissue. Increased flow
almost makes up
for decreased
oxygen carrying
capacity
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5
Q

causes of decraesed arterial oxygen saturation

A 
 High altitude
 Pneumonia
 Carbon monoxide
poisoning
 Cyanide poisonin
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6
Q

Precapillary Sphincters

A

 Open and close multiple times each minute
 As duration of open phase increases, flow through the tissue increases
 Duration of open phase inversely proportional to oxygen content and
directly proportional to concentration of metabolic waste

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7
Q

Theories for Acute Regulation

 Oxygen (nutrient) lack theory

A

 Oxygen & other nutrients needed for smooth muscle
contraction
 Nutrients not available – muscle relaxes producing dilation
 As metabolism increases local decrease in oxygen content
results in vasodilation

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8
Q

Theories for Acute Regulation Vasodialator theory

A

 As metabolism increases production / concentration of
metabolic waste increases
 Metabolic waste interacts with smooth muscle resulting in dilation

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9
Q

both Oxygen (nutrient) lack theory and Vasodialator theory

A

affect tone of smooth muscle mainly in metarterioles

and precapillary sphincters with some affect on arterioles

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10
Q

Overall tone of arterioles depends

A

on tone of autonomic nervous system

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11
Q

vasodilator factor release proportional to

A

tissue metabolism

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12
Q

on tone of autonomic nervous system

A

overall concentration of vasodilator factors. Factors cause direct dilation of metarterioles & precapillary sphincters.

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13
Q

Adenosine

A

 vasodilator Released from tissue in response to decreased oxygen
concentration
 Released by cardiac cells when coronary blood flow
inadequate, oxygen concentration has decreased, & stores of
ATP has decreased.

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14
Q

Carbon dioxide

A

potent vasodilator especially in the brain

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15
Q

Adenosine phosphate compounds

A

 Result of increased ATP degradation. vasoldilator

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16
Q

histamine

A

potent vasodilator released from mast cells & basophils

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17
Q

Hydrogen ions

A

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

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18
Q

potassium

A

vasodilator

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19
Q

Active Hyperemia

A

Response to increased metabolic demand with a tissue
 Example
 Increased metabolic activity of skeletal muscle

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20
Q

Reactive Hyperemia

A

 Response of tissue to period of no flow (ischemia)
 Flow can increase 4 to 7 times normal
 Longer the ischemic period the longer the reactive hyperemic period
 How long it takes to repay the oxygen debt

21
Q

Autoregulation: Response to
Changes in Mean Arterial
Pressure

A 
 Local control mechanisms are
only functional as long as MAP
doesn’t change
 If MAP changes then all tissues
will be affected by a change in
flow – All tissues would see some
type of local control response
 Able to keep flow through tissue
close to normal over
autoregulatory range
 Metabolic theory / Myogenic
theory
22
Q

Myogenic Theory

A

 Sudden stretch of small blood vessels causes
surrounding smooth muscle of vessel wall to contract
 Increased blood pressure stretches small blood
vessels triggering reactive constriction thus reducing
blood flow
 Decreased blood pressure results in decreased stretch
of small blood vessels triggering reactive relaxation
and increased blood flow
 Only allows vessels to respond to changes in
pressure, not changes in flow

23
Q

Endothelial-Derived Control Factors

A

 Nitric oxide: important direct vasodilator

 Endothelin: potent vasoconstrictor

24
Q

nitric oxide

A

Lipophilic gas released in response to variety of chemical
(increased calcium, angiotensin II) & physical stimuli (increased
shear stress due to increased flow)

25
Q

nitric oxide location of action

A

Acts mainly in larger vessels upstream of metarterioles &
precapillary sphincters –When flow through capillary increases
release of NO causes corresponding dilation of the larger upstream
vessels
 Decreased NO release is one consequence of chronic hypertension
or atherosclerosis

26
Q

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

A

 Has a half-life of 6 seconds – move into smooth muscle quickly
 Activates soluble guanylate cyclase (SGC)
 SGC mediates conversion of cyclic guanosine triphosphate (cGTP)
to cyclic guanosine monophosphate (cGMP)
 cGMP activates cGMP-dependent protein kinase (PKG)
 PKG ultimately leads to relaxation of the smooth muscles

27
Q

Endothelin

A

 Large amino acid peptide
 Small quantities produce significant vasoconstriction
 Present in all endothelial cells but concentration
increases with vessel injury
 Released from damaged cells
 Can close arterial vessels as large as 5 mm in diameter

28
Q

Local control is very quick but

A

not complete
 Not able to completely compensate and return blood flow to
normal level

29
Q

Chronic increase in metabolism

A

– flow will increase close to
actual need – long-term changes would bring total tissue
flow up to actual flow needed

30
Q

increase pressure from 100 to 150 mmHg (no change in

metabolism) would cause

A

Quick increase in blood flow – Within 30
seconds to 2 minutes local constriction occurs producing
slow decrease in flow through tissue – When compensation
complete, flow will still be 10 to 15% higher than needed

31
Q

If change in pressure was permanent,

A

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

32
Q

Short-term changes able to attenuate

A

changes in flow over pressure range of 75

mmHg to 175 mmHg

33
Q

Long-term changes able to keep flow

A

normal over pressure range of 50 to 250

mmHg

34
Q

long term control-change vascularity caused by

A

changes in metabolism or pressure. increase metabolism increase vascularity. decreases pressure increase vascularity. occurs in days chronic lox oxygen also increases vascularity. total change depends on max blood flow needed by tissue which allows response to exercise

35
Q

Vascular Endothelial Growth Factors

A

Small peptides that promote new vessel growth from
existing vessels
 Vascular endothelial growth factor (VEGF)
 Fibroblast growth factor
 Angiogenin
 Decrease of tissue oxygen leads to production by
affected cells

36
Q

Antiangiogenic Substances

A

Block the growth of new vessels
 Angiostatin
 Endostatin
 Not sure what they do within the body, BUT receiving
a lot of interest as anticancer agents
 Cancer cells cannot grow into tumors unless they are
able to develop an adequate blood supply

37
Q

Collateral Circulation

A

 Development of new vascular vessels to reestablish
blood flow to tissue affected by blocked arteries or
veins
 Involve opening of existing but closed pathways and
generation of new pathways
 If vessel blockage occurs slowly, then collateral
development could ensure adequate distal flow

38
Q

Norepinephrine

A

 Potent constrictor – released via ANS and adrenal medullae

39
Q

Epinephrine

A

 Not as potent as norepi

40
Q

Angiotensin II

A

 1/1,000,000 gram can increase arterial pressure 50 mmHg

 Part of the overall regulation of blood pressure

41
Q

 Vasopressin (Antidiuretic hormone)

A

More powerful than Angiotensin II
 Released from posterior pituitary
 Major role is to increase water reabsorption by the kidneys
 May play vasoactive role during acute hypovolemia

42
Q

Bradykinin

A

 Kinins are small peptides split from alpha2-globulins by
proteolytic enzymes
 Kallikrein is proteolytic enzyme in the blood – inactive
 Activated by damage to blood, inflammation
 Activated kallikrein interacts with alpha2-globulin to release kallidin
 Kallidin is converted by tissue enzymes to bradykinin
 Causes powerful vasodilation & increased capillary
permeability – important responses during inflammation

43
Q

 Histamine

A

 Released by mast cells and basophils located in damaged or
inflamed tissue
 Potent vasodilator & increases capillary permeability
 Can result in significant edema formation
 Common component of allergic reactions

44
Q

calcium

A

vasoconstriction

45
Q

potassium

A

vasodilation

46
Q

magnesium

A

vasodilation

47
Q

hydrogen ions

A

increases cause constriction and decreases cause dilation

48
Q

acetate citrate

A

cause mild vasodilation

Physiology (27 decks)

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