Perinatal profile of ventricular overload markers in congenital diaphragmatic hernia
Autor(a) principal: | |
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Data de Publicação: | 2008 |
Outros Autores: | , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
Texto Completo: | http://hdl.handle.net/1822/61452 |
Resumo: | Background: In congenital diaphragmatic hernia (CDH), pulmonary hypertension increases right ventricle (RV) afterload, which could impair heart function and contribute to poor outcome for most affected infants. Nevertheless, the real significance of vascular pulmonary alterations in perinatal hemodynamics is largely unknown. It is defined that ventricular pressure overload induces increased myocardium gene expression of B-type natriuretic peptide (BNP) and components of the reninangiotensinogen and endothelin (ET)–1 systems. Our aim was to evaluate perinatal myocardium expression of these genes associated with ventricular pressure overload in a nitrofen-induced CDH rat model. Methods: In the nitrofen-induced CDH rat model, fetuses from dated pregnant Sprague-Dawley rats at 15.5, 17.5, 19.5 and 21.5 days postcoitum as well as newborn pups were assigned to 3 experimental groups: control, nitrofen (exposed to nitrofen, without CDH), and CDH (exposed to nitrofen, with CDH). Myocardial samples collected from the RV and left ventricle (LV) were processed for quantification of messenger RNA (mRNA) of BNP, angiotensinogen, and ET-1. Results: The perinatal expression of BNP, angiotensinogen, and ET-1 mRNA in the RV and LV of the control group revealed daily changes. During gestation, the expression of BNP and angiotensinogen mRNA underwent significant oscillation compared with control in both nitrofen-exposed fetuses, although we cannot identify significant differences between the nitrofen and CDH groups. After birth, we found a significant increasing expression of all studied genes only in the RV of CDH pups. Conclusions: Perinatal myocardial quantification of BNP, angiotensinogen, and ET-1 mRNA levels suggests that both nitrofen-exposed and control pups revealed prenatal variations of expression of the studied genes. Moreover, CDH is associated with significant molecular alterations only in the RV after birth. |
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Perinatal profile of ventricular overload markers in congenital diaphragmatic herniaAdaptation, BiologicalAngiotensinogenAnimalsBase SequenceBiomarkersEndothelin-1Gene ExpressionGenetic MarkersHeart VentriclesHernia, DiaphragmaticHypertension, PulmonaryMolecular Sequence DataMyocardiumNatriuretic Peptide, BrainPhenyl EthersRNA, MessengerRatsRats, Sprague-DawleyHernias, Diaphragmatic, CongenitalB-type natriuretic peptidecongenital diaphragmatic herniaheartpulmonary hypertensionScience & TechnologyBackground: In congenital diaphragmatic hernia (CDH), pulmonary hypertension increases right ventricle (RV) afterload, which could impair heart function and contribute to poor outcome for most affected infants. Nevertheless, the real significance of vascular pulmonary alterations in perinatal hemodynamics is largely unknown. It is defined that ventricular pressure overload induces increased myocardium gene expression of B-type natriuretic peptide (BNP) and components of the reninangiotensinogen and endothelin (ET)–1 systems. Our aim was to evaluate perinatal myocardium expression of these genes associated with ventricular pressure overload in a nitrofen-induced CDH rat model. Methods: In the nitrofen-induced CDH rat model, fetuses from dated pregnant Sprague-Dawley rats at 15.5, 17.5, 19.5 and 21.5 days postcoitum as well as newborn pups were assigned to 3 experimental groups: control, nitrofen (exposed to nitrofen, without CDH), and CDH (exposed to nitrofen, with CDH). Myocardial samples collected from the RV and left ventricle (LV) were processed for quantification of messenger RNA (mRNA) of BNP, angiotensinogen, and ET-1. Results: The perinatal expression of BNP, angiotensinogen, and ET-1 mRNA in the RV and LV of the control group revealed daily changes. During gestation, the expression of BNP and angiotensinogen mRNA underwent significant oscillation compared with control in both nitrofen-exposed fetuses, although we cannot identify significant differences between the nitrofen and CDH groups. After birth, we found a significant increasing expression of all studied genes only in the RV of CDH pups. Conclusions: Perinatal myocardial quantification of BNP, angiotensinogen, and ET-1 mRNA levels suggests that both nitrofen-exposed and control pups revealed prenatal variations of expression of the studied genes. Moreover, CDH is associated with significant molecular alterations only in the RV after birth.ElsevierUniversidade do MinhoBaptista, Maria João Ribeiro LeiteSilva, Cristina Isabel NogueiraAreias, José CarlosCorreia-Pinto, Jorge2008-042008-04-01T00:00:00Zinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/1822/61452eng0022-34681531-503710.1016/j.jpedsurg.2007.08.04418405707info:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2023-07-21T12:18:52Zoai:repositorium.sdum.uminho.pt:1822/61452Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T19:11:42.768331Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse |
dc.title.none.fl_str_mv |
Perinatal profile of ventricular overload markers in congenital diaphragmatic hernia |
title |
Perinatal profile of ventricular overload markers in congenital diaphragmatic hernia |
spellingShingle |
Perinatal profile of ventricular overload markers in congenital diaphragmatic hernia Baptista, Maria João Ribeiro Leite Adaptation, Biological Angiotensinogen Animals Base Sequence Biomarkers Endothelin-1 Gene Expression Genetic Markers Heart Ventricles Hernia, Diaphragmatic Hypertension, Pulmonary Molecular Sequence Data Myocardium Natriuretic Peptide, Brain Phenyl Ethers RNA, Messenger Rats Rats, Sprague-Dawley Hernias, Diaphragmatic, Congenital B-type natriuretic peptide congenital diaphragmatic hernia heart pulmonary hypertension Science & Technology |
title_short |
Perinatal profile of ventricular overload markers in congenital diaphragmatic hernia |
title_full |
Perinatal profile of ventricular overload markers in congenital diaphragmatic hernia |
title_fullStr |
Perinatal profile of ventricular overload markers in congenital diaphragmatic hernia |
title_full_unstemmed |
Perinatal profile of ventricular overload markers in congenital diaphragmatic hernia |
title_sort |
Perinatal profile of ventricular overload markers in congenital diaphragmatic hernia |
author |
Baptista, Maria João Ribeiro Leite |
author_facet |
Baptista, Maria João Ribeiro Leite Silva, Cristina Isabel Nogueira Areias, José Carlos Correia-Pinto, Jorge |
author_role |
author |
author2 |
Silva, Cristina Isabel Nogueira Areias, José Carlos Correia-Pinto, Jorge |
author2_role |
author author author |
dc.contributor.none.fl_str_mv |
Universidade do Minho |
dc.contributor.author.fl_str_mv |
Baptista, Maria João Ribeiro Leite Silva, Cristina Isabel Nogueira Areias, José Carlos Correia-Pinto, Jorge |
dc.subject.por.fl_str_mv |
Adaptation, Biological Angiotensinogen Animals Base Sequence Biomarkers Endothelin-1 Gene Expression Genetic Markers Heart Ventricles Hernia, Diaphragmatic Hypertension, Pulmonary Molecular Sequence Data Myocardium Natriuretic Peptide, Brain Phenyl Ethers RNA, Messenger Rats Rats, Sprague-Dawley Hernias, Diaphragmatic, Congenital B-type natriuretic peptide congenital diaphragmatic hernia heart pulmonary hypertension Science & Technology |
topic |
Adaptation, Biological Angiotensinogen Animals Base Sequence Biomarkers Endothelin-1 Gene Expression Genetic Markers Heart Ventricles Hernia, Diaphragmatic Hypertension, Pulmonary Molecular Sequence Data Myocardium Natriuretic Peptide, Brain Phenyl Ethers RNA, Messenger Rats Rats, Sprague-Dawley Hernias, Diaphragmatic, Congenital B-type natriuretic peptide congenital diaphragmatic hernia heart pulmonary hypertension Science & Technology |
description |
Background: In congenital diaphragmatic hernia (CDH), pulmonary hypertension increases right ventricle (RV) afterload, which could impair heart function and contribute to poor outcome for most affected infants. Nevertheless, the real significance of vascular pulmonary alterations in perinatal hemodynamics is largely unknown. It is defined that ventricular pressure overload induces increased myocardium gene expression of B-type natriuretic peptide (BNP) and components of the reninangiotensinogen and endothelin (ET)–1 systems. Our aim was to evaluate perinatal myocardium expression of these genes associated with ventricular pressure overload in a nitrofen-induced CDH rat model. Methods: In the nitrofen-induced CDH rat model, fetuses from dated pregnant Sprague-Dawley rats at 15.5, 17.5, 19.5 and 21.5 days postcoitum as well as newborn pups were assigned to 3 experimental groups: control, nitrofen (exposed to nitrofen, without CDH), and CDH (exposed to nitrofen, with CDH). Myocardial samples collected from the RV and left ventricle (LV) were processed for quantification of messenger RNA (mRNA) of BNP, angiotensinogen, and ET-1. Results: The perinatal expression of BNP, angiotensinogen, and ET-1 mRNA in the RV and LV of the control group revealed daily changes. During gestation, the expression of BNP and angiotensinogen mRNA underwent significant oscillation compared with control in both nitrofen-exposed fetuses, although we cannot identify significant differences between the nitrofen and CDH groups. After birth, we found a significant increasing expression of all studied genes only in the RV of CDH pups. Conclusions: Perinatal myocardial quantification of BNP, angiotensinogen, and ET-1 mRNA levels suggests that both nitrofen-exposed and control pups revealed prenatal variations of expression of the studied genes. Moreover, CDH is associated with significant molecular alterations only in the RV after birth. |
publishDate |
2008 |
dc.date.none.fl_str_mv |
2008-04 2008-04-01T00:00:00Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/1822/61452 |
url |
http://hdl.handle.net/1822/61452 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
0022-3468 1531-5037 10.1016/j.jpedsurg.2007.08.044 18405707 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Elsevier |
publisher.none.fl_str_mv |
Elsevier |
dc.source.none.fl_str_mv |
reponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação instacron:RCAAP |
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Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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RCAAP |
institution |
RCAAP |
reponame_str |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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1799132549570625536 |