Control of capillary blood flow Flashcards

(30 cards)

1
Q

On the simplest level how is capillary flow regulated?

A

Arteriolar resistance

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2
Q

What are the 3 factors that regulate arteriolar resistance?

A
  1. Nerves
  2. Hormones and other vasoactive substances
  3. Local tissue metabolism
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3
Q

CO is proportional to what other measure?

Why is this?

A

VO2 (Volume of oxygen used per minute)

Blood flow is very well matched to metabolic demand

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4
Q

Why is VO2 used as a proxy for CO in studies of athletes?

A

It is proportional to CO

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5
Q

What equation is used to calculate flow in a capillary?

What is this simplified to?

Why can it be simplified?

A

Q = (PA - PV) / (Rpre + Rcap + Rpost)

Q α 1/Ra

Pressure gradient is fairly constant

Arteriolr resistance makes up 70% of total series and is the only directly regulated resistance

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6
Q

What is the purpose of LOCAL control of arteriolar resistance?

A

Matches local blood flow to local metabolici demand

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7
Q

What is the purpose of central autonomic contol of arteriolar resistance?

A

Controls TPR to maintain a constant ABP

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8
Q

What mechanisms of regulation are used in central control of arteriolar resistance?

A

Neuronal and endocrine

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9
Q

How is arteriolar smooth muscle arranged?

A

Radially

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10
Q

How is tension of vascular smooth muscle modulated?

A

Intracellular Ca2+ concentration

Phosphorylation of myosin light chain kinase

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11
Q

How is functional hyperaemia meausured?

A

Inflated cuff above arterial pressure around arm for 10 minutes

Cuff removed and an increase in blood flow through the arm is recorded

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12
Q

What metabolic factors promote vasodilatation of systemic arterioles?

A

Changes accompanying increased metabolism or normal metabolism with reduced blood flow:

-Reduced PO2

-Increased CO2

  • Decreased pH
  • Increased adenosine
  • Increased extracellular K+
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13
Q

Why does a large increase in pressure only result in a small increase in flow to areas such as the brain, heart and kidney?

A

Resistance increases as vessels vasoconstrict

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14
Q

What are the direct and indirect effects of an increased ABP on vasoconstriction?

A

DIRECT:

vasoconstriction via the mygogenic mechanism (increased pressure = increased resistance to prevent rapid rise in flow)

INDIRECT:

increased perfusion washes out local metabolites responsible for vasodilatation

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15
Q

How was the role of the endothelium in regulating vasuclar responses first observed?

A

ACh could only dilate arteries when endothelium was intact

(whereas noradrenaline constricted them even if the endothelium had been removed)

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16
Q

What is the signalling pathway from the endothelium to vasuclar smooth muscle?

A

ACh and bradykinin (a vasodilator peptide) stimulate NO production by the action of NO synthase on L-arginine in the endothelium

NO is lipophilic and so diffuses quickly, stimulating soluble guanylyl cyclase in the vascular smooth muscle

cGMP dependent protein kinase then phosphorylates MLCK, inhibiting it

17
Q

How does sildenafil (viagra) cause vasodilatation?

A

Inhibits cGMP-specific phosphodiesterase type 5 which reduces cGMP breakdown thus increasing MLCK inhibition

18
Q

Why does endothelial dysfucnction lead to atherosclerosis and increased riskk of clots?

A

Endothelium containd pro-coagulants, anti-coagulants, fibrinolytics, antibacterials and growith factors

19
Q

What is fibrinolysis?

A

A process that prevents blood clots from growing and becomming problematic

20
Q

Where are α1 receptors not found?

A

Brain, heart and placenta

21
Q

How does activation of an α1 receptor trigger Ca2+ release from the SR?

A

α1 receptor linked to the G-protein, Gαq

activates phospholipase C and raises IP3

22
Q

What are eicosanoids?

A

arachidonic acid derivativesinvolved in clotting and inflammatory responses

23
Q

What enzyme synthesises most eicosanoids?

Why is this of clinical significance?

A

Cyclooxygenase

This enzyme is inhibited by aspirin

24
Q

Which prosaglandins are vasoconstrictory?

25
Which prosaglandins are vasodilatory?
PGs I, D and E
26
What is thromboxane A2?
An eicosanoid produced by platelets that is reponsible for vasoconstriction and platelet aggregation
27
Which eicosanoid opposes thromboxane A2?
Prostacyclin (PG I2)
28
Why is aspirin used to treat myocardial infarction?
Asprin irreversibly blocks cyclo-oxygenase (COX-1) which is required by both thromboxane A2 and prostacyclin Endothelial cells have nuclei but platlets don't therefore the endothelium can synthesise more COX-1 to produce prostacyclin Thromboxane A2 not produced so there is a reduced risk of clotting
29
Where are prostaglandins produced?
Endothelium
30