Regulation of cerebral circulation Flashcards
1
Q
Special requirements
A
- grey matter is intolerant of hypoxia - without oxygen neuronal damage occurs within minutes - therefore needs a constant oxygen-rich blood supply
- brain has a very high oxygen consumption, so needs high blood flow
- local functioning in the brain gives changes in blood flow, so need to be able to change local blood flow according to need
2
Q
Brain adaptations
A
- high oxygen consumption / size
- high proportionof CO / size
- high resting oxygen extraction of 35% (body ave = 25%)
- brain is only 2% of body weight, but uses 20% of whole of body’s oxygen, although only gets 13% of CO
3
Q
Special features - structural
A
- CoW allows us to achieve a constant high blood flow of oxygen-rich blood
- the capillary density in the brain is very high - allows quick delivery and extraction of o2 to neurons
- Means that we can extract a lot more oxygene than we normally would be able to
- Have a BBB - formed of very tight epithelial juncitons
4
Q
Circle of willis
A
- Made of anterior cerebral artery, ICA, middle cerebral artery, posterior cerebral artery and posterior communicating arteries
- blood coming into brain will come from ICA or basilar artery
- clockages in CoW - can compensate as the blood can flow the other way around the circle
- blockages often come up ICA and end up in MCA
- these areas are most likely to be blocked - blocks motor cortex
5
Q
Special features - functional
A
- the brain controls the CVS, modulating sympathetic-mediated vasoconstriction to safeguard its own blood supply by:
>carotid sinus baroreceptors
>controlling heart and peripheral vasculature through reflexes - cerebral resistance vessels don’t constrict as a reflex
- auto-regulation is myogenic
- local metabolic vasodilation
- Tight BBB controls the access and outflow of solutes
6
Q
Carotid sinus baroreceptors
A
- Baroreflex - increase HR and contractility, increased vasoconstriciton and so TPR > increased BP
- increase in BP = prevents inhibitory signals > no baroreflex
- decrease in BP = stimulates inhibitory signals > baroreflex > increased BP
7
Q
Autoregulation
A
- as BP increases, blood flow is increased - at around 60mmHg it plateaus out
- as much as you increase it, the flow stays the same - distends the vessel > contraction of vessel, increase in vascular tone keeps flow the same
- Once you increase the pressure too high, the myogenic response doesn’t work and the vessel keeps distending
- if BP drops very low, you won’t be able to maintain BF to the brain - any small change in BP will mean a huge diff. in flow
- When you do a lot of activity, PCO2 increases. As CO2 levels increase, you get vasodilation in the brain - if you hyperventilate and blow off all the CO2, you get vasoconstriction
- When O2 levels decrease, you get local vasodilaiton, increasing BF and providing o2 to hypoxic area
8
Q
Regional hyperaemia
A
- when we do movements for example, the areas of the brain involved will have increased blood flow
- when a neuron fires a lot, there is a lot of K efflux and a lot of Na influx
- the ATPase is trying to control that, however you still get an EC build up of K
- This causes blood vessels to dilate - activates K channels > hyperpolarise the membrane > switch off VGCC > less contraction
- direct correlation between amount of firing and BF
9
Q
Nervous control of cerebral arteries
A
- peripheral arteries have lots of innervation from sympathetic nerves
- cerebral arteries within the brain have little innervation
- baroreflex doesnt really affect the cerebral vasculature
- C-fibres mediate pain of vascular headaches in strokes and later phase of migraine
> release dilators (subP and CGRP) and reduce constrictors (5-HT)
>Sumatriptan (used for migraines) is a 5-HT1b agonist - causes constriciton of blood vessels, reducing inflammation-induced vasodilation
10
Q
BBB
A
- continuous capillaries - very tight junctions, no fenestrations
- very selective carriers - not very leaky
11
Q
Function of BBB
A
- keep out = circulating neuro-active chemicals that would interfere with neuronal signalling (adrenaline etc)
- Keep in = NTs
- It is defective at some sites allowing access of circulating signalling molecules
> area postrema (vomiting centre)- emetic molecules allow us to get rid of toxins
> area of hypothalamus - angII > thirst sensation
> osmoreceptors of hypothalamus - ADH secretion
12
Q
Special problems of cerebral circulation
A
- postural hypotension
- vasospasm of cerebral artery - phase of migraine/following haemorrhagic stroke
- Strokes
- Space occupying lesions > increased intracranial pressure
13
Q
Space occupying lesions and Cushing’s reflex
A
- expands forcing brain down into foramen magnum
- forces activation of sympathetic vasoconstricotors
- increases TPR and so BP
- we try to switch this off, however wont work as it is constant force
- decrease HR - Bradycardia
- increased BP
14
Q
Postural hypotension
A
- when lying down there is a high CVP, high cardiac filling pressure and a large SV
- when standing, blood will pool in veins due to gravity
- less venous return, lower CVP, less load on heart
- less right SV, so less LV filling pressure, then less left SV
- decreases arterial pressure and so cerebral blood flow
- if this decreases too much we get under-perfusion in brain and dizziness
15
Q
Cerebral artery vasospasm
A
- very high K outside - membrane depolarises and causes vasoconstrictions and vasospasm
- SAH/intracranial haemorrhage can cause arterial vasospasm, leading to stroke
- caused by: 5-HT, neuropeptide Y, Endothelin-1, K+ ions
- reduced by: Ca channel blockers, ETa receptor blockers
