cerebral blood flow Flashcards
cerebral blood flow: explain the importance of cerebral blood flow regulation, list the neural and humoral factors involved in regulation, explain the regulatory mechanisms in response to changes in blood pressure and carbon dioxide tension
what happens when blood flow to brain is reduced by >50%
insufficient oxygen delivery, function becomes significantly impaired
what happens if total cerebral blood flow is interrupted for a) as little as 4 seconds, and b) after a few minutes
a) unconsciousness, b) irreversible damage occurs to brain
define syncope
fainting: common manifestation of reduced blood supply to brain
causes of syncope
hypotension, postural changes, vaso-vagal attack, sudden pain, emotional shock etc.
result of syncope
temporary interruption or reduction of blood flow to brain
what is the principal energy source of brain
glucose via blood
what % of the body’s glucose does the brain do
up to 50-60%
why does the brain use glucose
can’t store, synthesise or utilise any other source of energy; except in starvation where it metabolises ketones to a limited extent (CNS can adapt in chronic undernutrition)
common condition causing hypoglycaemia, and effects of hypoglycaemia
insulin-dependent diabetes (type 1); appear disorientated, slurred speech, impaired motor function
effect of [glucose] below 2nM
unconsciousness, coma, ultimately death
what mechanisms regulate cerebral blood flow
mechanisms affecting total cerebral blood flow, mechanisms relating activity to requirement in specific brain regions by altered localised blood flow
at what mean arterial blood pressure is total cerebral blood flow autoregulated
between approx. 60 and 160 mmHg
how is blood flow maintained
arteries and arterioles dilate or contract: stretch-sensitive cerebral vascular smooth muscle contracts at high blood pressure and relaxes at lower blood pressure
what happens below autoregulatory range
insufficient supply leads to compromised brain function
what happens above autoregulatory range
increased flow can lead to swelling of brain tissue which is not accomodated by “closed” cranium, increasing intracranial pressure
what determines O2 and glucose demands, and impact on autoregulation of blood supply
local brain activity, so must be local autoregulation
2 controls of local regulation of cerebral blood flow
neural, chemical
what do branches of surface pial vessles do
penetrate brain parenchyma and enter the CNS tissue (penetrating artioles and penetrating venules)
what do these branches of surface pial vessles branch to form, and function
capillaries which drain into venules and veins, then draining into surface pial veins
features of CNS vascularisation
densely vascularised (no neurone more than 100um from a capillary)
4 neural factors which regulate cerebral blood flow
sympathetic nerve stimulation, parasympathetic (facial nerve) stimulation, central cortical neurones, dopaminergic neurones
sympathetic nerve stimulation: location and effect
to main cerebral arteries, producing vasoconstriction (probably only when high arterial blood pressure)
parasympathetic (facial nerve) stimulation: effect
slight vasodilation
what do central cortical neurones release
vasoconstrictor neurotransmitters e.g. catecholamines (e.g. adrenaline, noradrenaline)
dopaminergic neurones: effect
vasoconstriction (localised effect relating to increased brain activity)
what do dopaminergic neurones (local effect) innervate
penetrating arterioles and pericytes around capillaries, causing contraction/relaxation and subsequent diversion
what are pericytes and what are their function
cells that wrap around capillaries; have diverse activities (e.g. immune function, transport properties, contractile)
function of dopaminergic neurones
local effect: diversion of cerebral blood to areas of high activity
effect of dopamine secreted by dopaminergic neurones
contraction of pericytes (in small vessels) via aminergic and serotoninergic receptors
examples of localised chemical factors that regulate cerebral blood flow by causing vasodilation
most clinically relevant: CO2 (indirect), pH; also: NO, K+. adenosine, anoxia, kinins, prostaglandins, histamine, endothelins
shape of pCO2 vs cerebral blood flow graph
sigmoid
how does a high pCO2 cause vasodilation of cerebral arteries, increasing blood flow
CO2 is derived from neural metabolic activity and combines with water to form HCO3- and H+ (via carbonic anhydrase) in cells, then enters vascular smooth muscle cells/pericytes; CO2 in blood also diffuses into vascular smooth muscle cells/pericytes and combines with water to form H+ (via carbonic anhydrase); finally H+ in blood cannot cross the BBB; all of this causes a decrease in pH, causing relaxation of contractile smooth muscle cells, increasing blood flow
imaging techniques because of local changes to cerebral blood flow
PET, functional MRI; increased neuronal activity = increased CO2 and subsequent H+ production = increased blood flow
what produces CSF in brain and where
regions of choroid plexus in cerebral ventricles; protects brain
CSF production: location and histology of cells
ependymal cells (epithelial-like glial cells, often ciliated) lining ventricles, aqueducts and canals, which in some regions of ventricles is modified to form branched villus structures (choroid plexus)
formation of CSF in choroid plexus: characteristics of capillaries and local ependymal cells
leaky capillaries (enters plasma via arachnoid granulations), but local ependymal cells have extensive tight junctions; secrete CSF into ventricles which then circulates
ventricles supplied by CSF via interventricular foramina
lateral and 3rd
ventricles supplied by CSF via cerebral aquaduct from 3rd
4th
pathway of CSF from 4th to circulation
into subarachnoid space via medial and lateral apetures
CSF volume
80-150ml
CSF functions
protection (physical and chemical), nutrition of neurones, transport of molecules
why is it clinically important that CSF has little protein
if high could indicate bacterial infection or damage to CSF vessels
