Hypoxic-Ischemic Brain Damage in 7-Days-Old Rats: Early Neuronal Changes and the Long-Term Outcome
Descripción del Articulo
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...
| Autores: | , , , , |
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| 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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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 |
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Universidad Nacional Mayor de San Marcos |
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UNMSM |
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UNMSM |
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Revistas - Universidad Nacional Mayor de San Marcos |
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Revistas - Universidad Nacional Mayor de San Marcos |
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La información contenida en este registro es de entera responsabilidad de la institución que gestiona el repositorio institucional donde esta contenido este documento o set de datos. El CONCYTEC no se hace responsable por los contenidos (publicaciones y/o datos) accesibles a través del Repositorio Nacional Digital de Ciencia, Tecnología e Innovación de Acceso Abierto (ALICIA).