Hypoxic-Ischemic Brain Damage in 7-Days-Old Rats: Early Neuronal Changes and the Long-Term Outcome

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OBJECTIVES: To study the changes after hypoxia-ischemia (HI), and to observe both, the vulnerability of the different regions of the brain to HI and the heat shock protein-72 kDa (HSP72) induction and its efects on the neuronal cell. MATERIAL AND METHODS: 7-days-old rats were exposed to left carotid...

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Autores: Ota Nakasone, Arturo, Ikeda, Tomoaki, Sameshima, Hiroshi, Ikenoue, Tsuyomu, Toshimori, Kiyotaka
Formato: artículo
Fecha de Publicación:1999
Institución:Universidad Nacional Mayor de San Marcos
Repositorio:Revistas - Universidad Nacional Mayor de San Marcos
Lenguaje:español
OAI Identifier:oai:ojs.csi.unmsm:article/4378
Enlace del recurso:https://revistasinvestigacion.unmsm.edu.pe/index.php/anales/article/view/4378
Nivel de acceso:acceso abierto
Materia:Brain Damage
Chronic
Cerebral Anoxia
Cerebral Ischemia
Immunohistochemistry
Lesión Cerebral Crónica
Anoxia Cerebral
Isquemia Cerebral
Inmunohistoquímica
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spelling Hypoxic-Ischemic Brain Damage in 7-Days-Old Rats: Early Neuronal Changes and the Long-Term OutcomeDaño Cerebral Hipóxico-Isquémico en Ratas de 7 Días de Edad: Alteraciones Neurológicas Tempranas y Lesiones PermanentesOta Nakasone, ArturoIkeda, TomoakiSameshima, HiroshiIkenoue, TsuyomuToshimori, KiyotakaBrain DamageChronicCerebral AnoxiaCerebral IschemiaImmunohistochemistryLesión Cerebral CrónicaAnoxia CerebralIsquemia CerebralInmunohistoquímicaOBJECTIVES: To study the changes after hypoxia-ischemia (HI), and to observe both, the vulnerability of the different regions of the brain to HI and the heat shock protein-72 kDa (HSP72) induction and its efects on the neuronal cell. MATERIAL AND METHODS: 7-days-old rats were exposed to left carotid artery ligation followed by 2 h of HI and then they were sacrificed at different time points. Brains extracted at 1-72 h were immunohistochemically study using the HSP-72 and the microtubule associated protein-2 (MAP2) stainings. Brains extracted at 1-4 weeks underwent histopathological study. RESULTS: Loss of MAP2 immunostaining was detected since the 1st hour post-insult, being highest at 24 h. MAP2 reappeared at 72 h in almost all the brain regions of the ligated hemisphere, except the hippocampal CA3 region. At 1-2 weeks post HI, we observed atrophic and cystic lesions. 15-20% of rats did not show any anatomical lesion up to 4 weeks post HI. The HSP72 synthesis was early in the dentate gyrus of the hippocampus, but a delayed induction was observed in the CA3 region; this region showed an increased vulnerability to HI. CONCLUSIONS: Absence of anatomical lesion was observed in 15-20% of rats exposed to HI. Atrophic or cystic lesions are observed since 1-2 weeks after the insult, despite an apparent immunohistochemical recovery at 72 h.OBJETIVOS: Observar las diferencias de vulnerabilidad de las diferentes regiones cerebrales frente a la hipoxia isquemia (HI), y la inducción de la síntesis de marcadores de injuria neuronal y su efecto posterior en la neurona. MATERIALES Y MÉTODOS: Se ligó la arteria carótida izquierda a ratas de 7 días de edad, seguido de 2 h de hipoxia, sacrificándolas a diferentes intervalos de tiempo. Se realizó un estudio inmunohistoquímico con la proteína del golpe del calor de 72 kDa (HSP72) y la proteína asociada al microtúbulo tipo 2 (MAP2) durante las primeras 72 h. RESULTADOS: La pérdida de inmunotinción del MAP2 se observó desde la 1 h, siendo máxima a las 24 h, pero a las 72 h se observó una reaparición en la mayoría de regiones del hemisferio izquierdo, excepto la región CA3 del hipocampo. Entre 1 y 2 semanas después se observó lesiones de tipo atrófico y cístico. 15-20% de ratas no sufrió daño anatómico hasta las 4 semanas. Hubo síntesis temprana de HSP72 en el giro dentado del hipocampo, mientras que en la región CA3 su inducción fue tardía, observándose aquí mayor vulnerabilidad a la HI. CONCLUSIONES: En 15 a 20% de ratas sometidas a HI no se observa daño anatómico hasta las 4 semanas. La lesión atrófica o cística se consolida entre 1 y 2 semanas después del insulto, a pesar de una aparente recuperación inmunohistoquímica a las 72 h.Universidad Nacional Mayor de San Marcos, Facultad de Medicina Humana1999-12-31info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://revistasinvestigacion.unmsm.edu.pe/index.php/anales/article/view/437810.15381/anales.v60i4.4378Anales de la Facultad de Medicina; Vol. 60 No. 4 (1999); 235-243Anales de la Facultad de Medicina; Vol. 60 Núm. 4 (1999); 235-2431609-94191025-5583reponame:Revistas - Universidad Nacional Mayor de San Marcosinstname:Universidad Nacional Mayor de San Marcosinstacron:UNMSMspahttps://revistasinvestigacion.unmsm.edu.pe/index.php/anales/article/view/4378/3496Derechos de autor 1999 Arturo Ota Nakasone, Tomoaki Ikeda, Hiroshi Sameshima, Tsuyomu Ikenoue, Kiyotaka Toshimorihttps://creativecommons.org/licenses/by-nc-sa/4.0info:eu-repo/semantics/openAccessoai:ojs.csi.unmsm:article/43782020-04-13T21:00:41Z
dc.title.none.fl_str_mv Hypoxic-Ischemic Brain Damage in 7-Days-Old Rats: Early Neuronal Changes and the Long-Term Outcome
Daño Cerebral Hipóxico-Isquémico en Ratas de 7 Días de Edad: Alteraciones Neurológicas Tempranas y Lesiones Permanentes
title Hypoxic-Ischemic Brain Damage in 7-Days-Old Rats: Early Neuronal Changes and the Long-Term Outcome
spellingShingle Hypoxic-Ischemic Brain Damage in 7-Days-Old Rats: Early Neuronal Changes and the Long-Term Outcome
Ota Nakasone, Arturo
Brain Damage
Chronic
Cerebral Anoxia
Cerebral Ischemia
Immunohistochemistry
Lesión Cerebral Crónica
Anoxia Cerebral
Isquemia Cerebral
Inmunohistoquímica
title_short Hypoxic-Ischemic Brain Damage in 7-Days-Old Rats: Early Neuronal Changes and the Long-Term Outcome
title_full Hypoxic-Ischemic Brain Damage in 7-Days-Old Rats: Early Neuronal Changes and the Long-Term Outcome
title_fullStr Hypoxic-Ischemic Brain Damage in 7-Days-Old Rats: Early Neuronal Changes and the Long-Term Outcome
title_full_unstemmed Hypoxic-Ischemic Brain Damage in 7-Days-Old Rats: Early Neuronal Changes and the Long-Term Outcome
title_sort Hypoxic-Ischemic Brain Damage in 7-Days-Old Rats: Early Neuronal Changes and the Long-Term Outcome
dc.creator.none.fl_str_mv Ota Nakasone, Arturo
Ikeda, Tomoaki
Sameshima, Hiroshi
Ikenoue, Tsuyomu
Toshimori, Kiyotaka
author Ota Nakasone, Arturo
author_facet Ota Nakasone, Arturo
Ikeda, Tomoaki
Sameshima, Hiroshi
Ikenoue, Tsuyomu
Toshimori, Kiyotaka
author_role author
author2 Ikeda, Tomoaki
Sameshima, Hiroshi
Ikenoue, Tsuyomu
Toshimori, Kiyotaka
author2_role author
author
author
author
dc.subject.none.fl_str_mv Brain Damage
Chronic
Cerebral Anoxia
Cerebral Ischemia
Immunohistochemistry
Lesión Cerebral Crónica
Anoxia Cerebral
Isquemia Cerebral
Inmunohistoquímica
topic Brain Damage
Chronic
Cerebral Anoxia
Cerebral Ischemia
Immunohistochemistry
Lesión Cerebral Crónica
Anoxia Cerebral
Isquemia Cerebral
Inmunohistoquímica
description OBJECTIVES: To study the changes after hypoxia-ischemia (HI), and to observe both, the vulnerability of the different regions of the brain to HI and the heat shock protein-72 kDa (HSP72) induction and its efects on the neuronal cell. MATERIAL AND METHODS: 7-days-old rats were exposed to left carotid artery ligation followed by 2 h of HI and then they were sacrificed at different time points. Brains extracted at 1-72 h were immunohistochemically study using the HSP-72 and the microtubule associated protein-2 (MAP2) stainings. Brains extracted at 1-4 weeks underwent histopathological study. RESULTS: Loss of MAP2 immunostaining was detected since the 1st hour post-insult, being highest at 24 h. MAP2 reappeared at 72 h in almost all the brain regions of the ligated hemisphere, except the hippocampal CA3 region. At 1-2 weeks post HI, we observed atrophic and cystic lesions. 15-20% of rats did not show any anatomical lesion up to 4 weeks post HI. The HSP72 synthesis was early in the dentate gyrus of the hippocampus, but a delayed induction was observed in the CA3 region; this region showed an increased vulnerability to HI. CONCLUSIONS: Absence of anatomical lesion was observed in 15-20% of rats exposed to HI. Atrophic or cystic lesions are observed since 1-2 weeks after the insult, despite an apparent immunohistochemical recovery at 72 h.
publishDate 1999
dc.date.none.fl_str_mv 1999-12-31
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://revistasinvestigacion.unmsm.edu.pe/index.php/anales/article/view/4378
10.15381/anales.v60i4.4378
url https://revistasinvestigacion.unmsm.edu.pe/index.php/anales/article/view/4378
identifier_str_mv 10.15381/anales.v60i4.4378
dc.language.none.fl_str_mv spa
language spa
dc.relation.none.fl_str_mv https://revistasinvestigacion.unmsm.edu.pe/index.php/anales/article/view/4378/3496
dc.rights.none.fl_str_mv https://creativecommons.org/licenses/by-nc-sa/4.0
info:eu-repo/semantics/openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/4.0
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Universidad Nacional Mayor de San Marcos, Facultad de Medicina Humana
publisher.none.fl_str_mv Universidad Nacional Mayor de San Marcos, Facultad de Medicina Humana
dc.source.none.fl_str_mv Anales de la Facultad de Medicina; Vol. 60 No. 4 (1999); 235-243
Anales de la Facultad de Medicina; Vol. 60 Núm. 4 (1999); 235-243
1609-9419
1025-5583
reponame:Revistas - Universidad Nacional Mayor de San Marcos
instname:Universidad Nacional Mayor de San Marcos
instacron:UNMSM
instname_str Universidad Nacional Mayor de San Marcos
instacron_str UNMSM
institution UNMSM
reponame_str Revistas - Universidad Nacional Mayor de San Marcos
collection Revistas - Universidad Nacional Mayor de San Marcos
repository.name.fl_str_mv
repository.mail.fl_str_mv
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