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Physio Exam 3 > L27 Local Control Of Blood Flow > Flashcards

L27 Local Control Of Blood Flow Flashcards

1
Q

Blood flow to an organ will

A

Increase or decrease depending on organ metabolism

Mechanisms: intrinsic or extrinsic

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2
Q

Intrinsic controllers of blood flow

A

Independent of neural and hormonal mechanisms

Inherent in tissue

Ex: auto regulation

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3
Q

Extrinsic control of blood flow

A

Hormonal/neural control

Sympathetic nervous system and various hormones

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4
Q

Blood flow to organs depends on

A

Interactions btw intrinsic and extrinsic factors

Local mechanisms have two main functions:

Maintain blood flow at constant level under resting conditions

Increase blood flow to a tissue to meet enhanced metabolic needs

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5
Q

Vascular smooth muscle tone

A

Contractile state of a resistance vessel= vessel tone

Basal tone= state of partial contraction independent of metabolic and neural mechanisms, results from properties of vessel (no external inputs at all)

Vessels can relax or contract further. Wide range of diameters

Resting state= most resistance vessels constricted somewhat more than basal due to sympathetic nerve activity (in vivo) greater than basal tone

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6
Q

Active vasoconstriction

A

A decrease in vessel diameter due to sympathetic stimulations or constrictor hormones/metabolites

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7
Q

Active vasodilation

A

An increase in vessel diameter due to dilator nerves, hormones, or local factors

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8
Q

Passive vasoconstriction

A

Return towards resting state from a dilated state due to the removal of active dilator influences

Passive = withdraw something

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9
Q

Passive vasodilation

A

Return towards resting state from a constricted state due to the removal of active constrictor influences

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10
Q

Intrinsic mechanisms

A

Auto regulation

Active(functional) hyperemia

Reactive hyperemia

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11
Q

Auto regulation

A

Blood flow to a tissue is maintained at a constant level over a physiological range of perfusion pressures

Independent of neural input

Flow maintained by altering the resistance to flow as perfusion pressure changes

Occurs without changes in metabolism

Pressure goes up, blood flow goes up briefly but back to normal by vessel altering its resistance

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12
Q

Metabolic theory of auto regulation

A

As perfusion pressure increases vasodilator metabolites are washed out of the surrounding interstitial fluid causing passive vasoconstriction and an increase in resistance (conversely vasodilation occurs as metabolites accumulate when pressure falls)

Increase pressure, increase Q, washout metabolic vasodilator, passive vasoconstriction, increase R

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13
Q

Myogenic theory of auto regulation

A

Increases in P cause increase in wall tension - vascular smooth muscle contracts- R increases

Conversely vasodilation occurs when P falls and wall tension decreases

Stretch sense Ca Channels open = stretch walls= Ca enters cell = contraction = increase R

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14
Q

Metabolic vasodilators

A

Do not enter the general circ at high enough conc to affect Q in other tissues

Vascular beds may differ in their responsiveness to various vasodilators

K+
CO2
Local hypoxia
Lactic acid
H+
Phosphate ions (extracellular) 
Prostaglandins * PGI2 PGE2
Adenosine 
Adenine nucleotides
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15
Q

Active (functional) hyperemia

A

Blood adjusted to meet metabolic demands of a tissue

As rate of metabolism increases, blood flow increase, due to increased production of vasodilator metabolites Which cause relaxation of vascular smooth muscle and a decrease in R

Active muscle needs more blood (only affects active bed of any tissue)

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16
Q

Reactive hyperemia

A

Increase in blood flow to a tissue that occurs in response to transient ischemia

Duration and magnitude of the hyperemia are proportional to time of ischemia

Due to local buildup of vasodilator metabolites during ischemic phase

Ex: weight lifting, cardiac circulation- during systole, heart contracts and obstructs blood flow into coronary artery, majority of perfusion occurs during diastole

17
Q

Extrinsic mechanisms

A

SNS

Hormones

18
Q

Neural control of vascular tone

Sympathetic adrenergic fibers

A

Control vascular R in most vascular beds

Precapillary resistance vessels are innervated by postganglionic nerves and release norepinephrine

Fibers tonically active in many vascular beds (vasoconstriction)

Contraction mediated via vascular smooth muscle alpah1 adrenergic receptors

SNS vasoconstriction May be attenuated by local vasodilator metabolites or mediators

Withdrawal of sympathetic activity = passive vasodilation

19
Q

Vasoactive hormones: epinephrine

A

Contract via alpha1 receptors on vascular smooth muscle of resistance vessels and veins

Relax via beta2 adrenergic receptors on vascular smooth muscle of resistance vessels (mainly skeletal muscle) ( epinephrines primary affinity is for beta2)

Net effect is dependent on epinephrine conc in plasma and relative conc/ affinity of receptors in a tissue

Most tissues = vasoconstriction;
Skeletal muscle = vasodilation due to higher conc beta2 receptors and a greater affinity of beta 2 for epinephrine

20
Q

Vasoactive hormones: angiotensin II

A

potent vasoconstrictor acts directly on vascular smooth muscle (AT1 receptors) of resistance vessels

Synthesized when blood pressure is low

Controls release of aldosterone from adrenal cortex

21
Q

Vasoactive hormones: vasopressin (AKA : AVP, ADH)

A

Peptide released from posterior pituitary in response to rising plasma osmolarity or low BP

Potent vasoconstrictor acts directly on vascular smooth muscle (V1 receptors) of resistance vessels

22
Q

Vasoactive substances and vascular tone

A

Some bind directly to receptors on VSM

Others bind to receptors on endothelial cells and cause release of vasoactive mediators which regulate VSM tone

Ex’s:
NO/vasodilator
PGI2, PGE2 : vasodilator
Endothelin : vasoconstrictor
Histamine: dilates arterioles/ constricts venules
Bradykinin: dilates arterioles/constricts venules

23
Q

Skeletal muscle circulation

A

Enormous range of Q in phasic muscle
33ml/min/kg at rest
1000ml/min/kg during exercise

Resistance vessels have high basal tone (myogenic)

24
Q

Role of skeletal muscle contraction in BP control

A

Large mass of tissue (40-45% weight)

Major site of resistance vessels

TPR regulated by controlling muscle R

Resistance influence by tonic vasoconstrictor activity, metabolic vasodilators, and regulation by reflex mechanisms (baroreceptors)

25
Q

Regulations of skeletal muscle Q: neural

A

Neural control dominates at rest

Tonic SNS vasoconstrictor activity (1Hz)
Alpha1 adrenergic receptor mediated (norepinephrine) TPR and BP can be maintained

Increase SNS activity (4-5Hz) can decrease Q by 70%

Vasodilation at rest is passive due to withdrawal of SNS activity

26
Q

Regulation of skeletal muscle Q

A

Metabolism (functional hyperemia)
With increased activity there is an increase in production of vasodilator metabolites
Vasodilator metabolites dominant during exercise ( although SNS activity may also be present)

Main vasodilators: K+, lactate, and adenosine

27
Q

Coronary circulation control of Q

A

Major role: local metabolites
Minor role: sympathetic innervation

Local metabolic vasodilators:
Hypoxia (decrease PO2)
Vasodilators (adenosine, NO, CO2, H+, prostaglandins)
Increase contractility = increase O2 demand/use= local hypoxia = vasodilation = increase Q (active hyperemia)

Auto regulation range: 50-60 mmHg to 150-160 mmHg

28
Q

Coronary circulation

Role of mechanical compression during systole I

A

Coronary vessels subject to compressive forces within wall of myocardium ( greater than in diastole)

Only about 20% total coronary flow occurs during systole

Compressive forces less marked in right ventricle due to smaller muscle mass and lower ventricular pressure development

29
Q

Coronary circulation

Reactive hyperemia

A

Brief occlusion of coronary vessel is followed by transient increase in coronary Q

Occlusion results in accumulation of vasodilator metabolites in interstitium

Magnitude / duration of extra flow dependent on duration of occlusion

30
Q

Coronary circulation

Neural considerations

A

Sympathetic stimulation:
Coronary arteries and arterioles
Norepinephrine- alpha1 - constrictor
Epinephrine - beta2 - vasodilation (minor one ventricles)

Heart
Beta1 - increase HR, contractility
Local metabolism- vasodilators- increase Q
In active heart, metabolic vasodilators overcome neural vasoconstriction

Net effect: increase Q to myocardium when SNS active

Physio Exam 3 (9 decks)

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