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17 Cards in this Set

  • Front
  • Back
global ischemia
cessation of blood flow to the entire brain
global ischemia damage time frame
less than 4 mins--no obvious damage following reperfusion
4-15 mins--death of specific neuronal populations
greater than 15 mins--necrosis occurs in brain
greater than 30 mins--large scale necrosis of brain
what is delayed neuronal death
vulnerable neurons die b/w 24-72 hours following reperfusion
most effective treatmen of global ischemic brain damage; decreases damaging reactions in brain tissue
main cause of ischemic damage
loss of ATP
ATP is zero by 4 mins
loss of ATP causes cessation of all ATP dependent processes in the brain
the most important being sodium/potassium atpase (ionic equilibrium)
consequence of disrupting state of neuronal cells
ions begin to equilibrate and ion gradients are lost
this results in net depolarization
ions that mediate necrosis during ischemia
if ischemia persists for greater than 20 mins, sodium influx causes cell swelling, lysis and death
less than 20mins, calcium influx causes the necrosis
what is excitotoxicity
influx of sodium and calcium during ischemia causes release of neurotransmitters, which further causes depolarization
damages that occurs w/ reperfusion
free radical production when oxygen is returned
protein synthesis is inhibited
overproduction of NO--contributes to further free radical damage
massive changes in gene transcription
activation of apoptosis
flow metabolism coupling
increase in neuronal activity leads to increase in local blood flow
what is the OGI
oxygen-glucose index
ratio of oxygen to glucose use
normal valus is 5.5
meaning that 5.5 molecules of oxygen are consumed for every 1 carbon of glucose utilized
how does OGI change when neuronal activity (and blood flow) increases
OGI decreases to about 4
so arteria-venous oxygen difference will be less in active brain regions
deoxyhemoglobin levels will be less in active brain regions
how does functional magnetic resonance imaging work
based on decrease in deoxyhemoglobin that occurs in active brain regions
so in active brain regions, fMRI signal will increase
extrinsic mechanism of cerebral blood flow autoregulation
baroreceptor relex--increase in MAP leads to vasodilation and decrease in MAP leads to vasoconstriction (via increase in sympathetic tone)
cerebral ischemic response--when pressure falls below 50mmgHg, CNS stimulates cardiovascular system to increase HR and CO
cushing reflex--increase intracranial pressure will cause MAP to increase, therefore increase in blood flow
intrinsic mechanism of cerebral blood flow autoregulation
arterial CO2--hypercapnia (vasodilation); hypocapnia (vasocontriction)
potassium ion
nitric oxide
all are vasodilators
neurogenic autoregulation
nitregic innnervation--postganglionic nerves innervating cerebral arteries; produces NO, which relaxes smooth muscles cholinergic--vasodilation via NO production
adrenergic--norepinephrine causes NO release, therefore vasodilation
myogenic autoregulation
stretch of smooth muscles causes muscle to contract