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CARDIOVASCULAR > 16 - Blood Flow Regulation II > Flashcards

16 - Blood Flow Regulation II Flashcards

1
Q

Example of shear detectors in the middle cerebral artery (brain):

A

-more flow=greater shear stress=reduction in diameter due to greater constriction

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2
Q

What is the pressure-flow interaction in the brain?

A

-flow induced constriction enhances efficiency of myogenic regulation
>works with it
-in other parts of the body they are competing

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3
Q

Flow-induced dilation in skeletal muscle vasculature (mechano-metabolic interaction):

A

-when dilate small arteries=increase flow through whole system
-when increase flow=shear stress increases=dilation
*helps facilitate increases in flow needed to meet O2 requirements
*dilation starts at muscle and goes ‘backwards’

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4
Q

What happens to diameter of an artery when the muscle contracts (increase pressure)?

A

-a single contraction for 1s vs. 5s = same dilation
-multiple contractions in 1s = more dilation (PHASIC contractions)
*compression-mediated dilation at the onset of exercise

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5
Q

Parabolic (laminar) flow pattern:

A

-velocity is fastest in the centre

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6
Q

Turbulent flow pattern:

A

-velocity is no longer lamina
>interferes with flow induced responses
Ex. may have more problems due to plague build up

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7
Q

Aortic stenosis and blood flow:

A

-laminar flow is already lost at the aorta
*shear patterns are disrupted
>influences with dilation and constriction responses
*exertional angina

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8
Q

Exertional angina is due to:

A

-increased LV work=increased LV pressure
>reduced SV and MAP
*compression of micro vessels of the year=impaired vasodilation=decrease inflow into coronary arterioles
-decreases vascular density=increase O2 diffusion distance

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9
Q

Metabolic signalling (intrinsic factor) at skeletal muscle:

A

-metabolites or signalling factors produced by or released nearby active tissue promotes VASODILATION
*counters extrinsic control (SNS)

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10
Q

What happens when muscles start contracting due to increased SNS?

A

-muscle contraction and results take over sympathetic input
>outcompete constriction and cause dilation=increased blood flow)
-kidneys: SNS in control= constriction happens

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11
Q

What are some metabolic signals at skeletal muscles?

A

-ACh
-ATP
-adenosine
-hypoxia
-CO2
-lactate
-H+
-K+
-etc.

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12
Q

What are some examples of metabolic signalling in/near skeletal muscle?

A

-ACh spillover from NMJ
-ATP released from RBC or adenosine production secondary to ATP metabolism
-decrease O2 or increase CO2 coupled with enhanced metabolism
-H+ or lactate accumulation with metabolism

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13
Q

What happens if you block one of the metabolic signalling mechanisms in the skeletal muscle?

A

-the other ones will pick up the slack
*no matter what you block, something will be the back up

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14
Q

Why is some ATP released from RBC?

A

-deform to make it through the vessels they deform
>releases ATP=causes dilation

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15
Q

Muscle blood flow over time

A

-phasic contractions
-contraction=constricts artery and blood flow is blocked
-relaxation=blood flow enters

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16
Q

Neurogenic metabolic signalling:

A

-NTs promote vasodilation
-ACh spillover from NMJ
-ATP or adenosine from neural and glial cell signalling
-5HT (serotonin) or GABA from neural and glial cell signalling
*brain and heart are always releasing NT that cause dilation

17
Q

What are some examples of NTs?

A

-ACh
-ATP
-adenosine
-NO
-5HT (serotonin)
-GABA

18
Q

Where is the relative responsiveness of myogenic mechanism?

A

-terminal arterioles

19
Q

Where is the relative responsiveness of flow dilation?

A

-more upstream than down stream

20
Q

Where is the relative responsiveness of metabolic dilation?

A

-terminal arterioles

21
Q

Where is the relative responsiveness of sympathetic constriction?

A

-terminal arterioles

22
Q

What is the effect of exercise on myocardial oxygen demand?

A

-change in demand comes from contraction (100%)
>60% change in HR
>40% change in contractility and LV work

23
Q

What is the effect of exercise on myocardial oxygen balance/supply?

A

-change in oxygen supply is primarily met by increase in coronary flow (80%)
>90% is from a decrease in coronary vascular resistance (dilating arteries)
>10% from perfusion pressure
*coronary perfusion increases with exercise intensity

24
Q

What is the relationship between left ventricular myocardial blood flow and heart rate?

A

-linear
>blood flow increases with HR
*HR is number one contributor to increase in O2 demand=is meet by increased coronary flow

25
Q

Endothelial signaling:

A

-intrinsic and extrinsic
-endothelium produces vasoactive factors that act on vascular smooth muscle
-serves in redistribution of blood flow to specific organs (vasodilation and vasoconstriction)
Ex. ET-1, NO

26
Q

Endothelial signaling: extrinsic part

A

-circulating factors/hormones interact with the endothelium

27
Q

Endothelial signaling: intrinsic part

A

-local hormones/peptides interact with endothelium
>vasoactive substances (NO or ET-1)

28
Q

Endo-mechanical interaction:

A

-during exercise, shear stress is increased and NO is produced
>more insulin and glucose delivery to muscle

29
Q

What happens during exercise: endo-mechanical interaction (extrinsic control)?

A

-insulin can bind and produce NO or ET-1 within endothelium
>ET-1: contraction
>NO: relaxation
*in an healthy animal=net production of NO=relaxation
>more flow to muscle=more insulin to muscle=better glucose uptake

30
Q

What happens if an animal is insulin resistant? (endothelial extrinsic pathway)

A

-shift to increase in ET-1 and reduce NO=promotes constriction
-can be reversed by exercise

31
Q

How can exercise ‘reverse’ insulin resistance?

A

-insulin pathway produces NO
>same pathway that shear stress works through
*increase shear stress in exercise and can condition it to respond to insulin and go back to dilation with insulin (instead of constriction)

32
Q

Endothelium-1 (ET-1):

A

-produced by endothelial cells
-diffuses and bind to ET receptors in smooth muscle=contraction
*net effect is constriction!

33
Q

NO pathway and drugs:

A

-central to promoting dilation

34
Q

Smooth muscle receptors:

A

-dilator and constrictors
>largest signal will prevail and dictate the tone of the vascular bed
*constantly producing ET-1 and NO in response to shear stress

35
Q

What are some examples of drugs to target changes in vascular tone?

A

-L-type Ca-channel blockers
-K-channel blockers
-alpha-adrenoceptor antagonist
-angiotensin receptor blocker
-ACE inhibitor
-renin inhibitor

CARDIOVASCULAR (17 decks)

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