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Cardiopulmonary Renal > Local Control Of Blood Flow > Flashcards

Local Control Of Blood Flow Flashcards

1
Q

What determines blood flow?

A

Tissue metabolic need

Increased metabolic activity correlated well with increased blood flow

Individual organs regulate own blood flow according metabolic requirements

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2
Q

What are the 2 factors affecting local control of blood flow?

A 
Extrinsic 
Tone- TPR
HR
MAP= CO * TPR
Controlled by nerves/hormones

Intrinsic/local control
Flow to organ capillaries controlled by arteriole vasoconstriction. Independent of nerves/hormone

Intrinsic/local control
-most impt in renal, cerebral and coronary
Less so in skel muscle
Little to none in skin

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3
Q

Summarize metabolic control of blood flow

A
  1. Metabolic (Active, functional) hyperemia
  2. Reactive (post-ischemic) hyperemia

Increased tissue metabolism—> increased release of vasodilator metabolites, endothelial secretions and paracrines—> vasodilation of blood vessels—> increased blood flow —> increased supply of oxygen, and nutrients as long as metabolism is increased

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4
Q

What is metabolic (active) hyperemia?

A

Increase in blood flow to an organ due to an increase production of vasodilator metabolites and endothelial secretions

Explains the increase in blood flow to skeletal and cardiac muscle during exercise

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5
Q

Describe reactive (post-ischemic) hyperemia

A

Temporary occlusion of a blood vessel—> build up of metabolites downstream of the occlusion—>vasodilation downstream—> increased blood flow

The longer the period of occlusion the longer the subsequent hyperemia

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6
Q

Describe myogenic control of blood flow

A

Blood flow is indirectly proportional to MAP (Bulk flow or Darcy’s law)
If MAP rises, blood flow is expected to increase

But between MAP of 60/80-160 mm Hg there is NO appreciable increase in blood flow (flow regulated)

Myogenic response. It is responsible for autoregulation of blood flow.

  • stretch of blood vessel wall (by increased pressure)
  • contraction of the smooth muscle of resistance arterioles
  • decreased radius, increased resistance
  • keep blood flow constant
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7
Q

What is the myogenic response for decreased blood pressure?

A

If blood pressure drops (moves to left)-vasoconstriction to reduce flow

If blood pressure increases (moves to right)-vasoconstriction to reduce blood flow

Important kidney and brain

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8
Q

Where is autoregulation most important?

A

Autoregulation most important in resistance arterioles of:

  • cerebral circulation
  • renal circulation
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9
Q

What is the function of autoregulation in myogenic control?

A

Safeguards blood flow to individual organs when BP falls

Stabilizes capillary perfusion pressure (prevents edema should BP rise)

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10
Q

What are the metabolic vasodilators?

A

Adenosine

H+

Low PaO2(hypoxia)

Interstitial K+

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11
Q

How is adenosine metabolic vasodilator?

A

Formed from AMP (particularly in skeletal and cardiac muscles). Good correlation between metabolic rate in cardiac muscle, adenosine content and coronary blood flow. (In renal constrictor)

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12
Q

How is H+ a metabolic vasodilator?

A

Cerebral blood vessels very senstive change PCO2 and [H+]. Arterial pCO2 important regulator of cerebral blood flow.

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13
Q

How is low PaO2(hypoxia) a metabolic vasodilator?

A

PaO2 normally about 100 mm Hg. PaO2<40 mm Hg—> vasodilation increase in blood flow helps to restore the oxygen supply to the tissue. Exception: lungs -hypoxia constrits pulmonary vessels

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14
Q

Why is interstitial K+ a metabolic vasodilator?

A

Skeletal muscle & brain activity—> increased K+ with increased action potentials. Skeletal muscle [K+]o increase from 4 mM —> 9mM. Increased K+ —> paradoxical relaxation of Vascular smooth muscle-(vasodilation) and increased blood flow

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15
Q

What is reactive (post-ischemic) hyperemia?

A

Hypoxia

Hypoxia —> vasodilation

  • activation of different K+ channels (KATP and Kir).
    • hyperpolarization abd L-type Ca2+ channel closure

-Vascular myocytes (smooth muscles) relax in hypoxia

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16
Q

Explain the paradoxical effect of hyperkalemia

A

Hyperkalemia due to increased activity of cardiac/skeletal muscles- local increases in K+ ions. Local control of blood flow via vasodilation of smooth muscle (active hyperemia)

Most cells: hyperkalemia reduces driving force, thus decreased K+ efflux and membrane depolarization

Paradoxical effect in smooth muscle: depolarization NOT occur! Hyperkalemia reduces driving force BUT opens special K+ channels! Increased conductance of K+ activated K+ channels offsets reduced driving force. Thus membrane doesn’t depolarize.

K+ activated K+ channels & hyperkalemia

  • Channel conductance via channel, and Na/K pump activity increased
  • Increased K+ ion efflux, offsets decreased DF, stabilizes Vm near Ek or hyperpolarized cell membrane

Closure of L-type Ca2+ channels

-Smooth muscle relaxation (recall some resting tone exists in vasculature smooth muscle )

17
Q

Contrast paradoxical effect in smooth muscle and normal cells

A

In normal cells: Hyperkakemia is an increase in K+ on the outside of the cell . Thus decreases the driving force and causes the RMP more positive. Depolarization can occur even quicker

Smooth muscle: hyperkalemia ow still an increase of K+ on the outside of the cell. This transiently decreases but it’s offset by the special K+ channels

Depolarization dies not occur in this case Because K+ leaves cell via special K+ channels —> hyperpolarization —> vasodilation

18
Q

Explain endothelial control of blood flow

A

Paracrine agents: endothelial cells secreted and act on adjacent myocytes.

Prostacyclin (PGI2) Vasodilator

  • a prostaglandin
  • inhibits platelet aggregation
  • produced in response to thrombin

Both NO (or EDHF) and prostacyclin limit spread of platelet aggregation and prevent uncontrolled vascular thrombosis

NO- vasodilator (formerly endothelium derived hyperpolarizing factir(EDHF) or EDRF; R= relaxing

Main stimulus for NO production= shear stress at endothelial cell (detected by glycocalyx on endothelial lumen)

Stimulates guanylyl Cyclase —> increased cGMP—> vasodilation

Continually modulates basal vascular tone

Responsible for:

  • flow induced vasodilation of exercise
  • vasodilation of erection
  • vasodilation of infkammation
19
Q

What hormones are involved in endothelial control of blood?

A

Circulating hormones

Paracrine hormones

Shearing forces

Hypoxia

E.g, acetylcholine, bradykinin, histamine via H1receotirs, VIP, substance P

20
Q

Describe endothelin control of blood flow

A

Endothelin (ET-1)-vasoconstrictor

Contributes to basal vascular tone

Associated with pathological states

Increased endothelin levels found in:

  • Hypoxia: partly responsible fir pulmonary hypertension seen at high altitudes.
  • Preeclampsia (acute hypertension of pregnancy)
  • cardiac failure: may contribute to the characteristic renal and peripheral vasoconstriction
  • Strokes: levels are increased in the CSF following subarachnoid hemorrhages, brain injury. Contributes to cerebral vasospasm

Migraines: likely increase cerebral pressure abd play a role in migraines

21
Q

How does NO activate smooth muscle relaxation ?

A

Paracrine activity of NO

  • ligand act on endothelial cells
  • NO generated via NO synthase activity on L-arginine
  • NO diffuses to vascular SM cell
  • Increased cGMP
    • decreased Ca2+ concentration
    • relaxation of vascular smooth muscle
    • vasodilation
22
Q

What is the role of NO in inflammation and endotoxins shock?

A

Results from specific activation of inducible NOS (iNOS) , which has higher activity than endothelial NOS)eNOS)

Inflammatory response: bradykinin, substance P, thrombin activate both endothelial NOS (eNOS) and inducible NOS(iNOS) (increased NO)

bacterial response: stimulates monocytes and macrophages release of interferon-gamma- a potent stimulator of iNOS (increased NOS)
-Can result in severe hypertension- endotoxin shock

23
Q

How can angina be treated?

A

Angina pectoris- poor blood flow to the heart

Nitrate drugs: nitroglycerin (glyceryl trinitrate), generates NO via aldehyde dehydrogenase. (Also used as an explosive)

24
Q

What is the mode of action of nitroglycerin/ glyceryl trinitrate in treating angina?

A

Increased cGMP—> vasodilation (venodilation> arteriolar dilation)

Venodilation leads to decreased CVP which leads to decreased preload (EDV) which then leads to decreased SV

Decreased S., decreases oxygen demand of heart muscle

Uses: angina pectineus- poor blood flow to heart

25
Q

What is the significance of Thromboxane as a vasoconstrictor?

A

Prostaglandin: thromboxane A2(vasoconstrictor): platelets from aravhifknic acud via COX. Involved in clotting and helps to stop bleeding. Inappropriate platelets activation —> thromboxane release can cause coronary vasospasm

Clinical box- thrombosis: clot within blood vessel

Thromboxane—> platelet aggregation

Aspirin (in low doses) inhibits Thromboxane formation in platelets

Aspirin—> prevent thrombosis in coronary atheroma

26
Q

What autocoid vasoconstrictors act through paracrine control of blood flow?

A

Serotonin 5HT (vasoconstrictor)

Prostaglandin (vasodilator/vasoconstrictor )(discussed I’m endothelial section

27
Q

What us function of Serotonin 5HT (vasoconstrictor) ?

A

Paracrine blood flow- from platelets during clotting- vasoconstriction (stops the bleeding ).

Coronary circulation: atheromatous coronary arteries: inappropriate platelet activation—> 5-HT release can cause coronary vasospasm

Cerebral circulation: partly responsible cerebral vasospasm (migraine, following a subarachnoid hemorrhage)

28
Q

What autocoids act as vasodilators in paracrine control of blood flow?

A

NO

Histamine (vasodilator): from mast cells —> inflammatory response. Dilated arterioles and constricts veins and increase venular permeability. Redness abd edema of inflammation

Bradykinin (vasodilator ): stimulates nociceptors abd is a potent algogen (pain producer). Via nitric oxide (NO)

Prostaglandin: prostacyclin/PGI2, PGE2 (vasoconstrictors): released from endothelial cells

29
Q

What is the sympathetic effect on blood flow?

A

Tonic sympathetic activity on blood vessels—> partially constructed
Decreased sympathetic activity—> vasodilation
Increased sympathetic tone—> vasoconstriction

Sympathetic tone in one organ can be regulated independently of other tissues

30
Q

Describe parasympathetic activity

A

Limited distribution to blood vessels

Release ACh which binds to muscuranic receptors

Activation of M receptors —> increased NO —> vasodilation

31
Q

Contrast the effects of epinephrine and norepinephrine on blood flow

A

Plasma conc. EPI: B2 - vasodilation, increased. HR, decreased TPR, increased CO, little change in MAP

NE- vasoconstriction a1, increased HR

Acts on a1 and B1 receptors

On graph, transient increase in HR (B1 receptors)
HR later decreases (baroceptor reflex)

32
Q

What is the main differentiation in epinephrine and nkrep?

A

Epinephrine can cause BITH vasodilation and vasoconstriction

Differential action of epinephrine on a and B receptors due to concentration

At normal plasma concentrations of epinephrine: preferentially binds B2 receptor—> vasodilation (in liver/ skeketal muscle), increased HR, and decreased TPR

Drug concentrations epinelhrine (higher than physiological ): preferentially binds a1 receptor—> vasoconstriction

(And at normal concentrations is causes vasoconstriction skin abd splachnic/gut circulations)

33
Q

Differentiate intrinsic and extrinsic regulation

A

Intrinsic- autoregulation- control of LOCAL blood flow at local/ organ arteriole level. Satisfy tissue/ organ metabolic demand

Extrinsic regulation- mainly concerned with control of mean arterial pressure (MAP) and TPR. Maintain blood pressure to ALL parallel arteries for tissue/organ perfusion

Cardiopulmonary Renal (35 decks)

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