Week 10- CVD and Neuro Flashcards
how cerebral ischamia leads to the neuronal and non neuronal death
cerebral ischameia–>imm cell infiltration(t cells, macrophages, microglial acitvation)–> release of inflamm cytokines–>neuronal and non neuronal cell death
after stroke the BBB becomes…
leaky
The order of imm cell infiltration after stroke
1.microglia( as theyre already local)
2.macrophages from blood or spleen
both within 24hrs
3.neutrophils(first reposnders above micropglia levels, prbably driven by 1 and 2 )
wihtin 48hrs
4. tcells (3 days)
5. b cells even less
When looking at infarct damage in SCID mice and normla mice
we see less infarct damage by about 30%. shows that whislt there may be low adaptive immune cells in the brian post stroke they can cause alot of damage.
How is an increase in astrocytes implicated in stroke response
increase in activated astorcytes–>when astrocytes beocme reactive they switch from support role to damaing ROS prodcuing–> forms glial scar whcihc can form an impenetrable layer to therpaies. start peaking within hours
How is an increase in macrophages implicated in stroke response
M2(antiinflamm) are thoguht to play mroe of a prominent role in the days to weeks after stroke
How is an increase in Treg cells are implicated in stroke response
thought to be benefical and have antiinflamm propertieis
in combo with other inflamm cells like M2, thought to aid in recovery
how much does spleen reduce after stroke
~50% after 3-4 days
When mice with splenectomy have MCAO performed, when compared with sham MCOA mice…
the amount fo infarct damage is significantly reduced. This makes sense as we know that inflamm contributes to about 30% of the damage
Do we see decrease in spleen weight at 24hrs and if we don’t when so we see it ?
we see slihglt decrease but not signficant. seen more at 72 hrs
How much apoptosis occurs in the spleen 24hrs and 72 hrs post-stroke?
quite alot at both time points but did not correlate wiht the trend for change in spleen weight.
We think this is because these cells have increased marker for apoptosis, so they’re in the process of dying but haven’t yet
clinical trials looking at antiinflamm use post ischaemic stroke…
were not successful in improving stroke outcome
How the immune system is implicated in hyper tension
increase in BP–> effect on brain–> increase in symp output–>effect on lymphoid tissue–>spleen released activated t cells into vasc–>rincrease in ROS–>endothelial damage–>hypertension and affect on organs like kidneys,adrnela cortex,glands–>affects Na+ and volume retension whic also contibtues to hypertension
RAG1 deficient mcie when put on an ang 2 infusion show…
blunted increase in blood pressure hsowing that increase BP is partly due to B and T cells
after any acutr stroke is raised blood pressure common?
yes
