Control of capillary blood flow Flashcards

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?

A

PG-F

25
Q

Which prosaglandins are vasodilatory?

A

PGs I, D and E

26
Q

What is thromboxane A2?

A

An eicosanoid produced by platelets that is reponsible for vasoconstriction and platelet aggregation

27
Q

Which eicosanoid opposes thromboxane A2?

A

Prostacyclin (PG I2)

28
Q

Why is aspirin used to treat myocardial infarction?

A

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
Q

Where are prostaglandins produced?

A

Endothelium

30
Q
A