Intracisternal application of endotoxin enhances the susceptibility to subsequent hypoxic-ischemic brain damage in neonatal rats.
Data(s) |
01/05/2003
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Resumo |
Perinatal brain damage is associated not only with hypoxic-ischemic insults but also with intrauterine inflammation. A combination of antenatal inflammation and asphyxia increases the risk of cerebral palsy >70 times. The aim of the present study was to determine the effect of intracisternal (i.c.) administration of endotoxin [lipopolysaccharides (LPS)] on subsequent hypoxic-ischemic brain damage in neonatal rats. Seven-day-old Wistar rats were subjected to i.c. application of NaCl or LPS (5 microg/pup). One hour later, the left common carotid artery was exposed through a midline neck incision and ligated with 6-0 surgical silk. After another hour of recovery, the pups were subjected to a hypoxic gas mixture (8% oxygen/92% nitrogen) for 60 min. The animals were randomized to four experimental groups: 1) sham control group, left common carotid artery exposed but not ligated (n = 5); 2) LPS group, subjected to i.c. application of LPS (n = 7); 3) hypoxic-ischemic study group, i.c. injection of NaCl and exposure to hypoxia after ligation of the left carotid artery (n = 17); or 4) hypoxic-ischemic/LPS study group, i.c. injection of LPS and exposure to hypoxia after ligation of the left carotid artery (n = 19). Seven days later, neonatal brains were assessed for neuronal cell damage. In a second set of experiments, rat pups received an i.c. injection of LPS (5 microg/pup) and were evaluated for tumor necrosis factor-alpha expression by immunohistochemistry. Neuronal cell damage could not be observed in the sham control or in the LPS group. In the hypoxic-ischemic/LPS group, neuronal injury in the cerebral cortex was significantly higher than in animals that were subjected to hypoxia/ischemia after i.c. application of NaCl. Injecting LPS intracisternally caused a marked expression of tumor necrosis factor-alpha in the leptomeninges. Applying LPS intracisternally sensitizes the immature rat brain to a subsequent hypoxic-ischemic insult. |
Formato |
application/pdf |
Identificador |
http://boris.unibe.ch/52747/1/Intracisternal%20Application%20of%20Endotoxin%20Enhances.pdf Coumans, Audrey B C; Middelanis, Johannes S; Garnier, Yves; Vaihinger, Hans-Martin; Leib, Stephen; Von Duering, Monika U; Hasaart, Tom H M; Jensen, Arne; Berger, Richard (2003). Intracisternal application of endotoxin enhances the susceptibility to subsequent hypoxic-ischemic brain damage in neonatal rats. Pediatric research, 53(5), pp. 770-775. Nature Publishing Group 10.1203/01.PDR.0000059221.40073.82 <http://dx.doi.org/10.1203/01.PDR.0000059221.40073.82> doi:10.7892/boris.52747 info:doi:10.1203/01.PDR.0000059221.40073.82 info:pmid:12621122 urn:issn:0031-3998 |
Idioma(s) |
eng |
Publicador |
Nature Publishing Group |
Relação |
http://boris.unibe.ch/52747/ |
Direitos |
info:eu-repo/semantics/restrictedAccess |
Fonte |
Coumans, Audrey B C; Middelanis, Johannes S; Garnier, Yves; Vaihinger, Hans-Martin; Leib, Stephen; Von Duering, Monika U; Hasaart, Tom H M; Jensen, Arne; Berger, Richard (2003). Intracisternal application of endotoxin enhances the susceptibility to subsequent hypoxic-ischemic brain damage in neonatal rats. Pediatric research, 53(5), pp. 770-775. Nature Publishing Group 10.1203/01.PDR.0000059221.40073.82 <http://dx.doi.org/10.1203/01.PDR.0000059221.40073.82> |
Palavras-Chave | #610 Medicine & health |
Tipo |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion PeerReviewed |