L12 Regulation of Vascular function Flashcards

1
Q

Where is the greatest change of vascular resistance able to be had in the vascular tree and where is the least

Why

A

The precapillary vessels (small arteries/arterioles) because they have proportionally greater thickness of the SM in tunica media

Post-capillary vessels have smaller proportion of VSM compared to matching pre capillary

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2
Q

What is the purpose of vasoconstriction in exercise? Is there
venoconstriction?

Which NS controls this and where is it

A
  • Sympathetic adrenergic nerves supply all vascular beds, distribution in pre and post capillary causing Vasoconstriction.

During exercise
- Arterial constriction helps to reduce blood flow through organ beds in GI tract to shunt more blood to muscle and skin (constriction offset by other means of dilation)

  • Venous constriction helps to increase flow to increase venous return to the heart
  • -> increasing SV to match increase in HR to get overall increase in CO.
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3
Q

What happens if you don’t increase venous return, only HR

A

The CO stays the same because the time for heart filling gets reduced so stroke volume decreases proportionally

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4
Q

What is the effect of increased precapillary resistance on the extrusion/ recovery of fluid from the capillaries

A
  1. Increased precapillary resistance
    - -> reduced post resistance flow
    - -> quicker drop in mean capillary hydrostatic pressure so that it goes below the mean pressure of interstitial fluid
    - -> Favours faster recovery of fluid back to capillary (collection of waste)

decreased resistance = more extrusion of fluids into tissues

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5
Q

List the 5 methods of local control of blood flow in bv at tissues

A

Autoregulation, Reactive hyperaemia (increase in blood), Myogenic hypothesis, Metabolic hypothesis,
Vascular endothelium hypothesis

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6
Q

What is Autoregulation

A

Innate ability of vessels to adapt to changes in perfusion pressure in order to maintain a normal blood flow

eg.
- If perfusion increases==> flow increases

  • triggers vasocontriction,
  • Resistance increases to reduce flow even though perfusion pressure is still high.
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7
Q

What is reactive hyperaemia

A
  1. Blood vessel occlusion for a short period is released
  2. Causes blood flow to rise above pre-occlusion level (hyperemia)
  3. This is maintained for period roughly proportional to duration of occlusion
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8
Q

What is Myogenic hypothesis

A
  1. Increased perfusion increases vascular pressure throughout circulation
  2. Increased transmural pressure leads to vascular distension
  3. Stretch elicits SM contraction
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9
Q

What is Metabolic hypothesis, where does it occur

  • not related to full circuit vasodilation
A

During exercise.

Vasodilation in bv in skeletal/cardiac muscle (precapillary vessels)

=> increase blood flow = nutrients to these tissues because of build up metabolites (from cardiac/skeletal muscle cells) in interstitial space which act on VSM.

Vasodilation triggers

  • ATP by product adenosine
  • inorganic phosphate from ATP use
  • Changes in osmolarity in the interstitial space
  • increased K+ extrusion from skeletal/cardiac cells due to high Na/K/ATPase.
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10
Q

What is the vascular endothelium hypothesis

A
  1. Increased blood flow increases shear stress on endothelium
  2. Leads to release of NO
  3. NO causes relaxation of VSM
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