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HOS Unit 2 > 23 Blood Flow Regulation > Flashcards

23 Blood Flow Regulation Flashcards

1
Q

What are the two vasoactive factors released from platelets and their functions?

A
  • Serotonin: Vasoconstriction, more platelet activation, and promoting NO release (vasodilation)
  • Thromboxane: Vasoconstriction, more platelet activation
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2
Q

What are the 3 endothelium-secreted vasoactive factors and their functions?

A
  • NO: vasodilation and platelet inhibition (Serotonin, ACh, or high flow (shear forces) stimulates its release. It is synthesized from L-arginine.)
  • Prostacyclin: vasodilation and platelet inhibition
  • Endothelin: powerful vasoconstrictor
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3
Q

How do the kidneys increase blood pressure? (pathway)

A
  • Renin-> Angiotensin 2 -> Constricts vessels

- (And fluid balance we will learn later)

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4
Q

What are the 3 determinants of cardiac work? How can cardiac work be estimated?

A
  • Contractility
  • Wall stress
  • Heart rate
  • Can be estimated: systolic arterial pressure X Heart Rate
  • (also recall that the isovolumetric phase of contraction is the most work-intensive)
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5
Q

What 7 methods are used to regulate blood flow to the heart?

A
  1. Metabolic regulation (vasodilator metabolites)
  2. Aortic pressure
  3. Neural and humoral (like hormonal) factors (strong indirect influence! Thru changes in cardiac workload (heart rate, wall stress, contractility) and metabolic demand)
  4. Paracrine factors (NO and prostacyclin)
  5. Coronary steal
  6. Extravascular compression (heart compresses its own vessels in left ventricle systole)
  7. The principle that guides all these is the need for O2 in the heart
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6
Q

Which things influence cerebral blood flow MOST? What 7 factors affect cerebral blood flow?

A
  • Primariy local metabolic, strong autoregulation, and CO2.
  • CO2 & H+ (biologically equivalent), O2, K+, adenosine, NO, and in cerebral ischemia the rest of the body will vasoconstrict to send extra blood to head
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7
Q

What is active versus reactive hyperemia? (a local vascular control)

A
  • Active=more blood due to increased tissue activity. (Tissue actually produces more vasodilator metabolites)
  • Reactive=more blood after ischemia (Less vasodilator metabolites are washed away by blood flow, concentration of them increases)
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8
Q

Describe the mechanism of each of the 2 methods of autoregulation? (a local vascular control)

A
  • Metabolic: Up pressure, up blood flow, up amt. of vasodilator metabolites being washed away.
  • Myogenic: Up volume, up stretch vascular smooth muscle (VSM), up Ca++ in VSM, smooth muscle contracts. (this is intrinsic property of smooth muscle)
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9
Q

What tissues is neurohumoral vascular control strong in? (such that it can override local control in these regions)

A
  • Skin
  • Resting skeletal muscles (primarily neural and myogenic at rest)
  • kidney (has good local control too though)
  • viscera
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10
Q

What tissues is neurohumoral vascular control weak in? (and thus local control dominates)

A
  • heart
  • brain
  • exercising skeletal muscle (primarily “local” vasodilator metabolites, a.k.a. hyperemia during exercise)
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11
Q

What are the 3 methods of “local” vascular control? What factors are used by each of these?

A
  • Autoregulation (myogenic, metabolic)
  • Hyperemia (vasodilator metabolites: K+, adenosine, prostaglandins, nitric oxide, hydrogen peroxide)
  • Paracrine factors (tonic NO, prostacyclin, serotonin, endothelin)
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12
Q

What are the 2 methods of “neurohumoral” vascular control?

A
  • Autonomic: Most important norepinephrine on alpha adrenergic receptors. Tonic & activate-able. Regionally selective.
  • Circulating vasoactive factors: Epi, NorEpi, angiotensin, vasopressin (ADH)
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13
Q

With atherosclerosis, what happens to the vasoconstriction response?

A

Greater response for same amt. chemical (NorEpi, serotonin, thromboxane)

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14
Q

Cutaneous circulation is controlled by what 2 methods?

A
  • Mostly neural

- Bit of local

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15
Q

Why is control of splanchnic circulation important to the body?

A

Helps determine TPVR (total peripheral vascular resistance) (sympathetic tone also determines TPVR)

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16
Q

How is normal blood flow maintained during changes in arterial pressure?

A

-Change vascular constriction/resistance by “local” autoregulation. Note that this does NOT significantly affect systemic blood pressure.

17
Q

What does Neuropeptide Y do to vessels?

A

Constrict

18
Q

What to beta-1, beta-2, and alpha adrenergic receptors do?

A
  • Respond to Norepinephrine and epinephrine as follows:
  • Alpha: Vasoconstrict (NorEpi or high Epi levels)
  • Beta-1:Up cardiac rate and contractility (NorEpi and Epi)
  • Beta-2: Vasodilate (unaffected by NorEpi. Low Epi levels at certain times in select vascular beds)
19
Q

What prevents norepinephrine release?

A
  • Vasodilators
  • Norepinephrine
  • Contracting skeletal muscle metabolites
20
Q

T/F Sympathetic tone influences both arteries and veins? What 2 effects does it have?

A
  • true

- constriction and decreased compliance

21
Q

Does NO or a decrease in sympathetic tone produce more vasodilation?

A

Decrease sympathetic tone does.

22
Q

What is the only major effect parasympathetics have on the circulatory system?

A

ACh binds muscarinic receptors on heart. (has almost no effect in vasculature, only rare vascular beds it vasodilates)

23
Q

Where is vasopressin (ADH) produced? Released? What does it do?

A
  • Hypothalamus
  • Posterior pituitary
  • Systemic vasoconstriction (like angiotensin II), down blood volume, down pressure, up osmolarity
24
Q

T/F left coronary artery pressure is highest during systole?

A

False. Diastole.

25
Q

Why is the brain in trouble at high altitude?

A

Because it relies on PCO2, not O2, to regulate its blood flow. Body hyperventilates to get enough O2. This decreases PCO2, preventing the CO2-induced vasodilation the brain needs to get enough O2. Result is syncope.

26
Q

Why do we give a brown paper bag to prevent syncope during hyperventilation?

A

Prevents CO2 level drop, preventing brain vasoconstriction to the point of not getting enough O2.

27
Q

How does skeletal muscle change its blood flow going from resting to exercise?

A
  • “Central command” as well as “ergoreceptor” signals from skeletal muscle cause up sympathetic tone (“exercise pressor reflex”)
  • 20-fold increase
  • Reserve capillaries perfused
  • Control switches (from neural/myogenic to local)
28
Q

How do we maintain B.P. when blood goes to muscle during exercise?

A
  • Sympathetic tone up everywhere else (HR and vasoconstriction)
  • Muscle venous pump (up venous return)
  • Hyperventilation creates negative thoracic pressure (up venous return)
29
Q

What organs receives 25% of cardiac output when resting?

A
  • Liver

- Brain

30
Q

How much blood volume is in the liver?

A
  • 15% total blood volume is here

- Portal vein is 70% of that, hepatic artery 30%

31
Q

T/F When we eat food, the brain signals for vasodilation of splanchnics?

A

False (Release of GI hormones is responsible)

32
Q

In cutaneous circulation, which areas are only sympathetically controlled?

A

Arteriovenous anastomoses

33
Q

In cutaneous circulation, which areas are mainly sympathetically controlled but also have autoregulation & hyperemia?

A

Arterioles (like many other places in the body!)

34
Q

In the skin, what are the mechanisms of vasoconstriction?

A
  • Local temp drop: Direct action on blood vessel & reflex-mediated (same for local temp increase)
  • Systemic temp. drop: hypothalamus ups sympathetic tone in skin

HOS Unit 2 (21 decks)

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