-
Je něco špatně v tomto záznamu ?
Time-dependent axonal impairment in experimental model of brain oedema
P. Kozler, V. Riljak, J. Pokorny
Jazyk angličtina Země Švédsko
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
20802439
Knihovny.cz E-zdroje
- MeSH
- analýza rozptylu MeSH
- axony patologie MeSH
- časové faktory MeSH
- edém mozku chemicky indukované patologie patofyziologie MeSH
- gyrus dentatus patologie patofyziologie MeSH
- hematoencefalická bariéra patologie patofyziologie MeSH
- krysa rodu rattus MeSH
- mannitol MeSH
- myelinová pochva patologie MeSH
- potkani Wistar MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
OBJECTIVES: Clinically very serious condition of ischaemia and brain injury which are often associated with brain oedema is frequently accompanied by the impairment of the structural integrity of axons. We wondered whether the brain oedema (without ischemia brain injury) can induce structural axonal impairment. METHODS: Brain oedema was induced by osmotic blood-brain barrier opening with 20% mannitol applied selectively into the internal carotid. Axonal changes were recognized as signs of myelin disintegration (oedematous vesicles, varicosity, myelin fragmentation) at histological sections stained with Black Gold in hippocampal areas CA1 and CA3 and in the dentate gyrus and cerebral cortex at time intervals of one hour, one day, three days and one week after the oedema induction. RESULTS: Impairment of the structural integrity was identified in myelin sheets in all areas studied in all experimental groups. Whereas in the control group axon were of the uniform diameter, in the experimental groups various forms of myelin disintegration were observed. The progression of myelin damage depended on the time elapsed after the oedema induction. CONCLUSION: Opening the blood-brain barrier with an osmotic insult induces brain oedema which represents a factor triggering axonal impairment accompanied with myelin changes. The development of axonal changes initiated by brain oedema only (without ischemia brain injury) is a novel observation.
- 000
- 00000naa a2200000 a 4500
- 001
- bmc12026137
- 003
- CZ-PrNML
- 005
- 20130110183527.0
- 007
- ta
- 008
- 120817s2010 sw f 000 0#eng||
- 009
- AR
- 035 __
- $a (PubMed)20802439
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a sw
- 100 1_
- $a Kozler, Petr $7 xx0057889 $u Department of Neurosurgery, First Medical Faculty, Charles University, Prague, Czech Republic.
- 245 10
- $a Time-dependent axonal impairment in experimental model of brain oedema / $c P. Kozler, V. Riljak, J. Pokorny
- 520 9_
- $a OBJECTIVES: Clinically very serious condition of ischaemia and brain injury which are often associated with brain oedema is frequently accompanied by the impairment of the structural integrity of axons. We wondered whether the brain oedema (without ischemia brain injury) can induce structural axonal impairment. METHODS: Brain oedema was induced by osmotic blood-brain barrier opening with 20% mannitol applied selectively into the internal carotid. Axonal changes were recognized as signs of myelin disintegration (oedematous vesicles, varicosity, myelin fragmentation) at histological sections stained with Black Gold in hippocampal areas CA1 and CA3 and in the dentate gyrus and cerebral cortex at time intervals of one hour, one day, three days and one week after the oedema induction. RESULTS: Impairment of the structural integrity was identified in myelin sheets in all areas studied in all experimental groups. Whereas in the control group axon were of the uniform diameter, in the experimental groups various forms of myelin disintegration were observed. The progression of myelin damage depended on the time elapsed after the oedema induction. CONCLUSION: Opening the blood-brain barrier with an osmotic insult induces brain oedema which represents a factor triggering axonal impairment accompanied with myelin changes. The development of axonal changes initiated by brain oedema only (without ischemia brain injury) is a novel observation.
- 650 _2
- $a analýza rozptylu $7 D000704
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a axony $x patologie $7 D001369
- 650 _2
- $a hematoencefalická bariéra $x patologie $x patofyziologie $7 D001812
- 650 _2
- $a edém mozku $x chemicky indukované $x patologie $x patofyziologie $7 D001929
- 650 _2
- $a gyrus dentatus $x patologie $x patofyziologie $7 D018891
- 650 _2
- $a ženské pohlaví $7 D005260
- 650 _2
- $a mužské pohlaví $7 D008297
- 650 _2
- $a mannitol $7 D008353
- 650 _2
- $a myelinová pochva $x patologie $7 D009186
- 650 _2
- $a krysa rodu Rattus $7 D051381
- 650 _2
- $a potkani Wistar $7 D017208
- 650 _2
- $a časové faktory $7 D013997
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a práce podpořená grantem $7 D013485
- 700 1_
- $a Riljak, Vladimír $7 xx0081611
- 700 1_
- $a Pokorný, Jaroslav
- 773 0_
- $w MED00168352 $t Neuro endocrinology letters $x 0172-780X $g Roč. 31, č. 4 (2010), s. 477-82
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/20802439 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y m
- 990 __
- $a 20120817 $b ABA008
- 991 __
- $a 20130110183635 $b ABA008
- 999 __
- $a ok $b bmc $g 948179 $s 783483
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2010 $b 31 $c 4 $d 477-82 $i 0172-780X $m Neuro-endocrinology letters $n Neuro-endocrinol. lett. $x MED00168352
- LZP __
- $a Pubmed-20120817/10/04