본문내용
이 nestin을 발현
4
II. experiment
1. 30 male wister rat
2.anesthesia → craniotomy
: sham-injury
: controlled cortical impact(CCI) :pneumatic piston ⇒ 4m/s, 2.5mm of compression
3. 48h after injury : IHC for nestin expression
III. result
1. 외상성 뇌 손상이후 병변 주변에서 nestin 발현
2. 국소적 뇌 허혈 이후에 관찰된 것과 유사
Brain Research 861(2000) 281-287 by Tae Chen et al
Brain lactate uptake increase at the site of impact after traumatic brain injury
I. Introduction
A. increased lactate levels in CSF, ECF
1. after traumatic brain injury
2. in cerebral ischemia
3. poor prognosis
4. impair postischemic recovery
B. after fluid percussion traumatic brain injury
1. TBI itself, not secondary ischemia : increased whole brain lactate, CSF lactate
2. depressed mitochondrial fucntion
3. facilitated anaerobic glycolysis : compensation
4. restoration of ionic homeostasis,
C. Lactate
1. energy substrate for damaged and premature neonatal brain
2. primarily fuels the recovery of synaptic function after hypoxia
3. better recovery than
D. purpose : test that
1. lactate can cross the BBB in sham and in TBI
2. lactate play a role in post-injury metabolic event
II. Materials and methods
A. experiment groups
1. 13 male Sprague-Dawley rat (356±26g)
1) TBI with 14C-lactate injection (n=8)
2) sham with 14C-lactate injection (n=5)
B. methods
1. cannulated femoral vein, artery.
2. brain microdialysis probe 설치
3. fluid percussion injury(FPI) : moderate magnitude of injury
4. 50μCi 14C-latate injuction
5. dialysate sample, blood sample
6. autoradiographic data
1)scarified 30min after injury
2)frozen, dried, exposed on film 40days
C. statistical analysis
1. ANOVA : microdialystate date, autoradiographic data
2. T-test : sham and injury group
III. Result
A. physiological variables : no differences
B. effect of lateral fluid percussion on brain 14C-lactate uptake
1. autoradiograph
1)sham : 14C-lactate uptake - evenly distributed through out the brain
2)TBI : 14C-lactate concentrated at the injury site
2.14C-lactate microdialisys compare
1)cortex : injury side>contralateral side, TBI 225% increase > normal
2)hippocampus : injury side>contralateral side
3. 14C-lactate radioactivity time course
1)blood sample : 5min-peak. after-decrease
2)brain dialysate : 20min peak. after-decrease
IV. Discussion
1. results due to
1) preferential, active lactate uptake
2) trasiently open BBB after injury
2. brain metabolization substrate
1) glucose : primary energy substrate of the CNS
2) alternative substrates : lactate, pyruvate
3) lactate : preferred over glucose as an energy substrate in neuron
3. TBI rat use lactate and preserve glucose in the ECF
4. TBI-increased glutamete : disturbed ionic homeostasis
:increased glutamate uptake by astrocytes stimulated the production of glycolytic lactate
5. during recovery from hypoxia : lactate conversion to pyruvate doesnot require investment of ATP
V. conclusion
1. injured brain take up peripheral lactate
2. sparing of ECF glucose for recovery of injuried brain tissue
4
II. experiment
1. 30 male wister rat
2.anesthesia → craniotomy
: sham-injury
: controlled cortical impact(CCI) :pneumatic piston ⇒ 4m/s, 2.5mm of compression
3. 48h after injury : IHC for nestin expression
III. result
1. 외상성 뇌 손상이후 병변 주변에서 nestin 발현
2. 국소적 뇌 허혈 이후에 관찰된 것과 유사
Brain Research 861(2000) 281-287 by Tae Chen et al
Brain lactate uptake increase at the site of impact after traumatic brain injury
I. Introduction
A. increased lactate levels in CSF, ECF
1. after traumatic brain injury
2. in cerebral ischemia
3. poor prognosis
4. impair postischemic recovery
B. after fluid percussion traumatic brain injury
1. TBI itself, not secondary ischemia : increased whole brain lactate, CSF lactate
2. depressed mitochondrial fucntion
3. facilitated anaerobic glycolysis : compensation
4. restoration of ionic homeostasis,
C. Lactate
1. energy substrate for damaged and premature neonatal brain
2. primarily fuels the recovery of synaptic function after hypoxia
3. better recovery than
D. purpose : test that
1. lactate can cross the BBB in sham and in TBI
2. lactate play a role in post-injury metabolic event
II. Materials and methods
A. experiment groups
1. 13 male Sprague-Dawley rat (356±26g)
1) TBI with 14C-lactate injection (n=8)
2) sham with 14C-lactate injection (n=5)
B. methods
1. cannulated femoral vein, artery.
2. brain microdialysis probe 설치
3. fluid percussion injury(FPI) : moderate magnitude of injury
4. 50μCi 14C-latate injuction
5. dialysate sample, blood sample
6. autoradiographic data
1)scarified 30min after injury
2)frozen, dried, exposed on film 40days
C. statistical analysis
1. ANOVA : microdialystate date, autoradiographic data
2. T-test : sham and injury group
III. Result
A. physiological variables : no differences
B. effect of lateral fluid percussion on brain 14C-lactate uptake
1. autoradiograph
1)sham : 14C-lactate uptake - evenly distributed through out the brain
2)TBI : 14C-lactate concentrated at the injury site
2.14C-lactate microdialisys compare
1)cortex : injury side>contralateral side, TBI 225% increase > normal
2)hippocampus : injury side>contralateral side
3. 14C-lactate radioactivity time course
1)blood sample : 5min-peak. after-decrease
2)brain dialysate : 20min peak. after-decrease
IV. Discussion
1. results due to
1) preferential, active lactate uptake
2) trasiently open BBB after injury
2. brain metabolization substrate
1) glucose : primary energy substrate of the CNS
2) alternative substrates : lactate, pyruvate
3) lactate : preferred over glucose as an energy substrate in neuron
3. TBI rat use lactate and preserve glucose in the ECF
4. TBI-increased glutamete : disturbed ionic homeostasis
:increased glutamate uptake by astrocytes stimulated the production of glycolytic lactate
5. during recovery from hypoxia : lactate conversion to pyruvate doesnot require investment of ATP
V. conclusion
1. injured brain take up peripheral lactate
2. sparing of ECF glucose for recovery of injuried brain tissue
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