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Page 1: The Cardiovascular System: Blood Vessels - · PDF fileChapter 19 The Cardiovascular System: ... 1/20/2016 23 . Figure 19.11 Direct and indirect (hormonal) mechanisms for renal control

© Annie Leibovitz/Contact Press Images

Chapter 19

The

Cardiovascular

System:

Blood Vessels

MDufilho 1/20/2016 1

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Review of Study Guide

• OYO – Blood Vessel Anatomy p. 699-706

• Physiology of Circulation p. 706

• Maintaining Systemic Blood Pressure p. 708

– Short-Term Mechanisms

• Neural Controls

• Hormonal Controls

– Long-Term Mechanisms

• Renal Regulation

• OYO IP CD: Autoregulation and Capillary Dynamics

• OYO – Homeostatic imbalances p. 716

• OYO – Circulatory Shock p. 717 and handout

1/20/2016 2 MDufilho

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Part 2 Physiology of Circulation

Definition of Terms

• Blood flow: volume of blood flowing through vessel, organ,

or entire circulation in given period

– Measured in ml/min, it is equivalent to cardiac output

(CO) for entire vascular system

• Blood pressure (BP): force per unit area exerted on wall of

blood vessel by blood

– Expressed in mm Hg

– Measured as systemic arterial BP in large arteries near

heart

– Pressure gradient provides driving force that keeps blood

moving from higher- to lower-pressure areas

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Definition of Terms (cont.)

• Resistance (peripheral resistance): opposition

to flow

– Measurement of amount of friction blood

encounters with vessel walls, generally in

peripheral (systemic) circulation

– Three important sources of resistance

• Blood viscosity

• Total blood vessel length

• Blood vessel diameter

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Relationship between Flow, Pressure, and

Resistance

• Blood flow (F) is directly proportional to blood

pressure gradient (P)

– If P increases, blood flow speeds up

• Blood flow is inversely proportional to peripheral

resistance (R)

– If R increases, blood flow decreases, so

F = P/R

• R is more important in influencing local blood

flow because it is easily changed by altering

blood vessel diameter

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Figure 19.6 Blood pressure in various blood vessels of the systemic circulation.

MDufilho

Systolic pressure

Mean pressure

Diastolic pressure

0

20

40

60

80

100

120

Blo

od

p

re

ssure (m

m H

g)

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Arterial Blood Pressure

• Determined by two factors:

1. Elasticity (compliance or distensibility) of

arteries close to heart

2. Volume of blood forced into them at any time

• Blood pressure near heart is pulsatile

– Rises and falls with each heartbeat

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Arterial Blood Pressure (cont.)

• Systolic pressure:

• Diastolic pressure:

• Pulse pressure:

• Pulse:

• Mean Arterial Pressure (MAP)

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Arterial Blood Pressure (cont.)

• MAP is calculated by adding diastolic pressure +

1/3 pulse pressure

– Example: BP = 120/80; Pulse Pressure =

120 − 80 = 40; so MAP = 80 + (1/3)40 = 80 +

13 = 93 mm Hg

• Pulse pressure and MAP both decline with

increasing distance from heart

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19.8 Regulation of Blood Pressure

• Maintaining blood pressure requires cooperation

of heart, blood vessels, and kidneys

– All supervised by brain

• Three main factors regulating blood pressure

– Cardiac output (CO)

– Peripheral resistance (PR)

– Blood volume

• Blood pressure varies directly with CO, PR, and

blood volume

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19.8 Regulation of Blood Pressure

• Remember:

F = P/R

and that F = CO, so substituting gives

CO = P/R

and rearranging,

P = CO R

• Shows that blood pressure (MAP) is directly

proportional to CO and PR

– Changes in one variable are quickly

compensated for by changes in other variables

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19.8 Regulation of Blood Pressure

• Recall that CO = SV HR, so if MAP = CO R,

then

MAP = SV HR R

• Anything that increases SV, HR, or R will also

increase MAP

– SV is effected by venous return (EDV)

– HR is maintained by medullary centers

– R is effected mostly by vessel diameter

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19.8 Regulation of Blood Pressure

• Factors can be affected by:

– Short-term regulation: neural controls

– Short-term regulation: hormonal controls

– Long-term regulation: renal controls

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Figure 19.9 Major factors

determining MAP.

MDufilho

Peripheral resistance

Diameter of blood vessels

Blood viscosity

Heart rate

Stroke volume

Blood vessel length

Cardiac output

Mean arterial pressure (MAP)

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Short-Term Regulation: Neural Controls

• Two main neural mechanisms control peripheral resistance

1. MAP is maintained by altering blood vessel diameter,

which alters resistance

• Example: If blood volume drops, all vessels constrict

(except those to heart and brain)

2. Can alter blood distribution to organs in response to

specific demands

• Neural controls operate via reflex arcs that involve:

– Cardiovascular center of medulla

– Baroreceptors

– Chemoreceptors

– Higher brain centers

• Goals?

MDufilho

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Short-Term Regulation: Neural Controls

(cont.)

• Baroreceptor reflexes

– Located in carotid sinuses, aortic arch, and walls

of large arteries of neck and thorax

– If MAP is high:

• Increased blood pressure stimulates baroreceptors to

increase input to vasomotor center

• Inhibits vasomotor and cardioacceleratory centers

• Stimulates cardioinhibitory center

• Results in decreased blood pressure

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Short-Term Regulation: Neural Controls

(cont.)

• Baroreceptor reflexes (cont.)

– If MAP is low:

• Reflex vasoconstriction is initiated that increases CO

and blood pressure

• Example: when a person stands, BP falls and triggers:

– Carotid sinus reflex: baroreceptors that monitor BP to

ensure enough blood to brain

– Aortic reflex maintains BP in systemic circuit

• Baroreceptors are ineffective if altered blood pressure

is sustained

– Become adapted to hypertension, so not triggered by

elevated BP levels

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Figure 19.10 Baroreceptor reflexes that help maintain blood pressure homeostasis.

MDufilho

Baroreceptors

in carotid sinuses and aortic arch

are stimulated.

Rate of

vasomotor impulses allows vasodilation,

causing R. CO and R

return blood pressure to

homeostatic range.

Sympathetic

impulses to heart cause HR,

contractility, and

CO.

Impulses from baroreceptors

stimulate cardioinhibitory center (and inhibit cardioacceleratory

center) and inhibit vasomotor center.

Stimulus:

Blood pressure (arterial blood

pressure rises

above normal range).

CO and R

return blood pressure to

homeostatic

range.

Vasomotor

fibers stimulate vasoconstriction,

causing R.

Stimulus:

Blood pressure (arterial blood

pressure falls below

normal range).

Baroreceptors

in carotid sinuses and aortic arch

are inhibited Sympathetic

impulses to heart Cause HR,

contractility, and

CO.

Impulses from baroreceptors

activate cardioacceleratory center (and inhibit cardioinhibitory center)

and stimulate vasomotor center.

Homeostasis: Blood pressure in normal range

2

3

4b

5

4a

1

5 4b

1

2

3

4a

Slide 6

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Short-Term Regulation: Neural Controls

(cont.) • Chemoreceptor reflexes

– Aortic arch and large arteries of neck detect increase in CO2, or drop

in pH or O2

– Cause increased blood pressure by:

• Signaling cardioacceleratory center to increase CO

• Signaling vasomotor center to increase vasoconstriction

• Influence of higher brain centers

– Reflexes that regulate BP are found in medulla

– Hypothalamus and cerebral cortex can modify arterial pressure via

relays to medulla

– Hypothalamus increases blood pressure during stress

– Hypothalamus mediates redistribution of blood flow during exercise

and changes in body temperature

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Short-Term Mechanisms: Hormonal Controls

• Hormones regulate BP in short term via

changes in peripheral resistance or long term

via changes in blood volume

• Adrenal medulla hormones

– Epinephrine and norepinephrine from adrenal

gland increase CO and vasoconstriction

• Angiotensin II stimulates vasoconstriction

• ADH: high levels can cause vasoconstriction

• Atrial natriuretic peptide decreases BP by

antagonizing aldosterone, causing decreased

blood volume

MDufilho

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Long-Term Mechanisms: Renal Regulation

• Baroreceptors quickly adapt to chronic high or

low BP so are ineffective for long-term

regulation

• Long-term mechanisms control BP by altering

blood volume via kidneys

• Kidneys regulate arterial blood pressure by:

1. Direct renal mechanism

2. Indirect renal mechanism (renin-angiotensin-

aldosterone)

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Long-Term Mechanisms: Renal Regulation

(cont.)

• Direct renal mechanism

– Alters blood volume independently of hormones

• Increased BP or blood volume causes elimination of

more urine, thus reducing BP

• Decreased BP or blood volume causes kidneys to

conserve water, and BP rises

– ADH

– Alcohol

MDufilho 1/20/2016 22

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Long-Term Mechanisms: Renal Regulation

(cont.)

• Indirect mechanism – The renin-angiotensin-aldosterone mechanism

• Decreased arterial blood pressure causes release of renin from

kidneys

• Renin enters blood and catalyzes conversion of angiotensinogen

from liver to angiotensin I

• Angiotensin-converting enzyme, especially from lungs, converts

angiotensin I to angiotensin II

– Angiotensin II acts in four ways to stabilize arterial BP and ECF:

• Stimulates aldosterone secretion

• Causes ADH release from posterior pituitary

• Triggers hypothalamic thirst center to drink more water

• Acts as a potent vasoconstrictor, directly increasing blood

pressure

MDufilho

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Figure 19.11 Direct and indirect (hormonal) mechanisms for renal control of blood pressure.

MDufilho

Arterial pressure

Blood volume

Aldosterone

Mean arterial pressure

Blood volume

Mean arterial pressure

Filtration by kidneys

Urine formation

Arterial pressure

Inhibits baroreceptors

Sympathetic nervous system activity

Water intake Water reabsorption

by kidneys

Sodium reabsorption

by kidneys

ADH release by

posterior pituitary

Vasoconstriction;

peripheral resistance Thirst via

hypothalamus Adrenal cortex

Angiotensin II

Angiotensin converting

enzyme (ACE)

Secretes

Initial stimulus

Physiological response

Result

Direct renal mechanism

Angiotensin I

Angiotensinogen

Renin release from kidneys

Indirect renal mechanism (renin-angiotensin-aldosterone)

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Clinical Applications

• ACE Inhibitors

• Nitroglycerin

• What if ?????? Worksheet.

1/20/2016 MDufilho 25

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Summary of Blood Pressure Regulation

• Goal of blood pressure regulation is to keep

blood pressure high enough to provide

adequate tissue perfusion, but not so high that

blood vessels are damaged

– Example: If BP to brain is too low, perfusion is

inadequate, and person loses consciousness

– If BP to brain is too high, person could have

stroke

MDufilho 1/20/2016 26

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Figure 19.12 Factors that increase MAP.

MDufilho

Activity of muscular pump and respiratory

pump

Fluid loss from hemorrhage,

excessive sweating

Crisis stressors: exercise, trauma,

body temperature

Baroreceptors

Release of ANP P

Vasomotor tone; bloodborne chemicals

(epinephrine, NE, ADH,

angiotensin II)

Dehydration, high hematocrit

Body size

Conservation of Na+ and

water by kidneys

Blood volume Blood pressure

Blood pH O2

CO2

Chemoreceptors Blood volume

Venous return

Activation of vasomotor and cardio- acceleratory centers in brain stem

Stroke volume

Heart rate

Diameter of blood vessels

Blood viscosity

Blood vessel length

Peripheral resistance Cardiac output

Mean arterial pressure (MAP)

Initial stimulus

Physiological response

Result

1/20/2016 27

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19.9 Control of Blood Flow

• Tissue perfusion: blood flow through body

tissues; involved in:

1. Delivery of O2 and nutrients to, and removal of

wastes from, tissue cells

2. Gas exchange (lungs)

3. Absorption of nutrients (digestive tract)

4. Urine formation (kidneys)

• Rate of flow is precisely right amount to provide

proper function to that tissue or organ

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19.9 Control of Blood Flow

• Rate of blood flow is controlled by extrinsic and intrinsic

factors

– Extrinsic control: sympathetic nervous system and

hormones control blood flow through whole body

• Act on arteriolar smooth muscle to reduce flow to

regions that need it the least

– Intrinsic control: Autoregulation (local) control of

blood flow: blood flow is adjusted locally to meet specific

tissue’s requirements

• Local arterioles that feed capillaries can undergo

modification of their diameters

• Organs regulate own blood flow by varying resistance

of own arterioles

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Figure 19.13 Distribution of blood flow at rest and during strenuous exercise.

MDufilho

Brain

Heart

Skeletal muscles

Skin

Kidneys

Abdomen

Other

750

250

1200

500

1100

1400

600

750

750

12,500

600

600

400

1900

Total blood flow during strenuous exercise 17,500 ml/min

Total blood flow at rest 5800 ml/min

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Autoregulation: Intrinsic (Local)

Regulation of Blood Flow

• Autoregulation: local (intrinsic) conditions that

regulate blood flow to that area

– Reactive hyperemia: increased blood flow to an

area due to intrinsic factors

• Two types of intrinsic mechanisms both

determine final autoregulatory response

– Metabolic controls

– Myogenic controls

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Autoregulation: Intrinsic (Local)

Regulation of Blood Flow (cont.)

• Metabolic controls

– Increase in tissue metabolic activities results in:

• Declining levels of O2

• Increasing levels of metabolic products (H+, K+,

adenosine, and prostaglandins)

– Effects of change in levels of local chemicals

• Cause direct relaxation of arterioles and relaxation of

precapillary sphincters

• Cause release of nitric oxide (NO), a powerful

vasodilator, by endothelial cells

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Autoregulation: Intrinsic (Local)

Regulation of Blood Flow (cont.)

• Metabolic controls (cont.)

• Endothelins, also released from endothelium, are

potent vasoconstrictors

• NO and endothelins are usually balanced unless

blood flow is inadequate, in which case NO wins

control, causing vasodilation

– Inflammatory chemicals can also cause

vasodilation

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Autoregulation: Intrinsic (Local)

Regulation of Blood Flow (cont.)

• Myogenic controls

– Myogenic responses: local vascular smooth

muscle responds to changes in MAP to keep

perfusion constant to avoid damage to tissue

• Passive stretch: increased MAP stretches vessel wall

more than normal

– Smooth muscle responds by constricting, causing

decreased blood flow to tissue

• Reduced stretch: decreased MAP causes less stretch

than normal

– Smooth muscle responds by dilating, causing increased

blood flow to tissue

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Autoregulation: Intrinsic (Local)

Regulation of Blood Flow (cont.)

• Long-term autoregulation

– Occurs when short-term autoregulation cannot

meet tissue nutrient requirements

• Long-term autoregulation may take weeks or months

to increase blood supply

– Number of vessels to region increases

(angiogenesis), and existing vessels enlarge

– Common in heart when coronary vessel

occluded, or throughout body in people in

high-altitude areas

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Figure 19.14 Intrinsic and extrinsic control of arteriolar smooth muscle in the systemic circulation.

MDufilho

Intrinsic controls

(autoregulation)

• Metabolic or myogenic controls

• Distribute blood flow to individual

organs and tissues as needed

Vasoconstrictors

Myogenic

• Stretch

Metabolic

• Endothelins

Sympathetic tone

Neural

Ho r monal

• Angiotensin II

• Antidiuretic hormone

• Epinephrine

• Norepinephrine

Extrinsic controls

• Neural or hormonal controls

• Maintain mean arterial pressure

(MAP)

• Redistribute blood during exercise

and thermoregulation

Metabolic

• Prostaglandins

• Adenosine

• Nitric oxide

O2

CO2

H+

K+

Neural

Hormonal

• Atrial natriuretic

peptide

Sympathetic tone

Vasodilators

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Figure 19.16 Blood flow velocity and total cross-sectional area of vessels.

MDufilho

50

40

30

20

10

0

5000

Relative cross- sectional area of different vessels of the vascular bed

4000

3000

2000

1000

0

Total area

(cm2) of the

vascular

bed

Velocity of

blood flow

(cm/s)

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Vasomotion

• Vasomotion: intermittent flow of blood through

capillaries

– Due to on/off opening and closing of precapillary

sphincters

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Figure 19.17-1 Capillary transport mechanisms.

MDufilho

Red blood cell in lumen

Endothelial cell

Intercellular cleft

Fenestration (pore)

Endothelial cell nucleus

Tight junction

Basement membrane

Pinocytotic vesicles

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Figure 19.17-2 Capillary transport mechanisms.

MDufilho

Basement membrane

Endothelial fenestration (pore)

Intercellular cleft

Pinocytotic vesicles

Caveolae

Transport via vesicles or caveolae (large substances)

Movement through fenestrations (water-soluble substances)

Movement through intercellular clefts (water-soluble substances)

Diffusion through membrane (lipid-soluble substances)

Lumen

3

2

1

4

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Focus Figure 19.1 Bulk fluid flow across capillary walls causes continuous mixing of fluid between the plasma and the interstitial fluid

compartments, and maintains the interstitial environment.

MDufilho

Piston

Venule

Arteriole

Lymphatic

capillary

Solute

molecules

(proteins) Boundary Boundary

Hydrostatic pressure (HP)

The big picture

Each day, 20 L of fluid filters from capillaries at their

arteriolar end and flows through the interstitial

space. Most (17 L) is reabsorbed at the venous end.

Recall from Chapter 3 (p. 71) that two kinds

of pressure drive fluid movement:

17 L of fluid per

day is reabsorbed

into the capillaries

at the venous end.

Fluid moves

through the

interstitial space.

For all capillary

beds, 20 L of fluid

is filtered out per

day—almost 7

times the total

plasma volume! Osmotic pressure (OP)

• Due to fluid pressing against a

boundary (e.g., capillary wall)

• HP “pushes” fluid across the

boundary

• In blood vessels, is due to

blood pressure

• Due to nondiffusible solutes

that cannot cross the boundary

• OP “pulls” fluid across the

boundary

• In blood vessels, is due to

plasma proteins

“Pushes” “Sucks”

About 3 L per

day of fluid

(and any leaked

proteins) are

removed by the

lymphatic

system (see

Chapter 20).

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Focus Figure 19.1-3 Bulk fluid flow across capillary walls causes continuous mixing of fluid between the plasma and the interstitial fluid

compartments, and maintains the interstitial environment.

MDufilho

HPif = 0 mm Hg

NFP = 10 mm Hg

HPc = 35 mm Hg

OPif = 1 mm Hg

OPc = 26 mm Hg

Osmotic pressure (OPif) in interstitial fluid “pulls” fluid out of capillary.

Hydrostatic pressure (HPif) in interstitial fluid “pushes” fluid into capillary.

Hydrostatic pressure in capillary (HPc) “pushes” fluid out of capillary.

Osmotic pressure in capillary (OPc) “pulls” fluid into capillary.

Boundary

(capillary wall)

Interstitial fluid Capillary lumen

How do the pressures drive fluid flow across a capillary?

Net filtration occurs at the arteriolar end of a capillary.

Let’s use what we know about pressures

to determine the net filtration pressure

(NFP) at any point. (NFP is the pressure

driving fluid out of the capillary.) To do

this we calculate the outward pressures

(HPc and OPif) minus the inward

pressures (HPif and OPc). So,

As a result, fluid moves from the

capillary into the interstitial space.

NFP = (HPc + OPif) (HPif + OPc)

= (35 + 1) (0 + 26)

= 10 mm Hg (net outward pressure)

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Focus Figure 19.1-4 Bulk fluid flow across capillary walls causes continuous mixing of fluid between the plasma and the interstitial fluid

compartments, and maintains the interstitial environment.

MDufilho

NFP= 8 mm Hg

HPif = 0 mm Hg

HPc = 17 mm Hg

OPc = 26 mm Hg

OPif = 1 mm Hg

Net reabsorption occurs at the venous end of a capillary.

Hydrostatic pressure in capillary “pushes” fluid out of capillary. The pressure has dropped because of resistance encountered along the capillaries.

Osmotic pressure in capillary “pulls” fluid into capillary.

Boundary (capillary wall)

Interstitial fluid

Hydrostatic pressure in interstitial fluid “pushes” fluid into capillary.

Osmotic pressure in interstitial fluid “pulls” fluid out of capillary.

Again, we calculate the NFP:

NFP = (HPc + OPif) (HPif + OPc)

= (17 + 1) (0 + 26)

= 8 mm Hg (net inward pressure)

Notice that the NFP at the venous end is a negative number. This means that reabsorption, not filtration, is occurring and so fluid moves from the

interstitial space into the capillary.

Capillary lumen

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Circulatory Shock OYO from handout

• Any condition in which

– Blood vessels inadequately filled

– Blood cannot circulate normally

• Results in inadequate blood flow to meet tissue

needs

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