Heart hypoplasia in an animal model of congenital diaphragmatic hernia
Autor(a) principal: | |
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Data de Publicação: | 2001 |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Revista do Hospital das Clínicas |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0041-87812001000600003 |
Resumo: | PURPOSE: In previous papers, we described a new experimental model of congenital diaphragmatic hernia in rabbits, and we also reported noninvasive therapeutic strategies for prevention of the functional and structural immaturity of the lungs associated with this defect. In addition to lung hypoplasia, pulmonary hypertension, biochemical, and structural immaturity of the lungs, the hemodynamics of infants and animals with congenital diaphragmatic hernia are markedly altered. Hence, cardiac hypoplasia has been implicated as a possible cause of death in patients with congenital diaphragmatic hernia, and it is hypothesized to be a probable consequence of fetal mediastinal compression by the herniated viscera. Cardiac hypoplasia has also been reported in lamb and rat models of congenital diaphragmatic hernia. The purpose of the present experiment was to verify the occurrence of heart hypoplasia in our new model of surgically produced congenital diaphragmatic hernia in fetal rabbits. METHODS: Twelve pregnant New Zealand rabbits underwent surgery on gestational day 24 or 25 (normal full gestational time - 31 to 32 days) to create left-sided diaphragmatic hernias in 1 or 2 fetuses per each doe. On gestational day 30, all does again underwent surgery, and the delivered fetuses were weighed and divided into 2 groups: control (non-surgically treated fetuses) (n = 12) and congenital diaphragmatic hernia (n = 9). The hearts were collected, weighed, and submitted for histologic and histomorphometric studies. RESULTS: During necropsy, it was noted that in all congenital diaphragmatic hernia fetuses, the left lobe of the liver herniated throughout the surgically created defect and occupied the left side of the thorax, with the deviation of the heart to the right side, compressing the left lung; consequently, this lung was smaller than the right one. The body weights of the animals were not altered by congenital diaphragmatic hernia, but heart weights were decreased in comparison to control fetuses. The histomorphometric analysis demonstrated that congenital diaphragmatic hernia promoted a significant decrease in the ventricular wall thickness and an increase in the interventricular septum thickness. CONCLUSION: Heart hypoplasia occurs in a rabbit experimental model of congenital diaphragmatic hernia. This model may be utilized for investigations in therapeutic strategies that aim towards the prevention or the treatment of heart hypoplasia caused by congenital diaphragmatic hernia. |
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Heart hypoplasia in an animal model of congenital diaphragmatic herniaCongenital diaphragmatic herniaHeartHypoplasiaFetusPURPOSE: In previous papers, we described a new experimental model of congenital diaphragmatic hernia in rabbits, and we also reported noninvasive therapeutic strategies for prevention of the functional and structural immaturity of the lungs associated with this defect. In addition to lung hypoplasia, pulmonary hypertension, biochemical, and structural immaturity of the lungs, the hemodynamics of infants and animals with congenital diaphragmatic hernia are markedly altered. Hence, cardiac hypoplasia has been implicated as a possible cause of death in patients with congenital diaphragmatic hernia, and it is hypothesized to be a probable consequence of fetal mediastinal compression by the herniated viscera. Cardiac hypoplasia has also been reported in lamb and rat models of congenital diaphragmatic hernia. The purpose of the present experiment was to verify the occurrence of heart hypoplasia in our new model of surgically produced congenital diaphragmatic hernia in fetal rabbits. METHODS: Twelve pregnant New Zealand rabbits underwent surgery on gestational day 24 or 25 (normal full gestational time - 31 to 32 days) to create left-sided diaphragmatic hernias in 1 or 2 fetuses per each doe. On gestational day 30, all does again underwent surgery, and the delivered fetuses were weighed and divided into 2 groups: control (non-surgically treated fetuses) (n = 12) and congenital diaphragmatic hernia (n = 9). The hearts were collected, weighed, and submitted for histologic and histomorphometric studies. RESULTS: During necropsy, it was noted that in all congenital diaphragmatic hernia fetuses, the left lobe of the liver herniated throughout the surgically created defect and occupied the left side of the thorax, with the deviation of the heart to the right side, compressing the left lung; consequently, this lung was smaller than the right one. The body weights of the animals were not altered by congenital diaphragmatic hernia, but heart weights were decreased in comparison to control fetuses. The histomorphometric analysis demonstrated that congenital diaphragmatic hernia promoted a significant decrease in the ventricular wall thickness and an increase in the interventricular septum thickness. CONCLUSION: Heart hypoplasia occurs in a rabbit experimental model of congenital diaphragmatic hernia. This model may be utilized for investigations in therapeutic strategies that aim towards the prevention or the treatment of heart hypoplasia caused by congenital diaphragmatic hernia.Faculdade de Medicina / Universidade de São Paulo - FM/USP2001-12-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0041-87812001000600003Revista do Hospital das Clínicas v.56 n.6 2001reponame:Revista do Hospital das Clínicasinstname:Universidade de São Paulo (USP)instacron:USP10.1590/S0041-87812001000600003info:eu-repo/semantics/openAccessTannuri,Ueniseng2002-02-05T00:00:00Zoai:scielo:S0041-87812001000600003Revistahttp://www.scielo.br/rhcPUBhttps://old.scielo.br/oai/scielo-oai.php||revista.hc@hcnet.usp.br1678-99030041-8781opendoar:2002-02-05T00:00Revista do Hospital das Clínicas - Universidade de São Paulo (USP)false |
dc.title.none.fl_str_mv |
Heart hypoplasia in an animal model of congenital diaphragmatic hernia |
title |
Heart hypoplasia in an animal model of congenital diaphragmatic hernia |
spellingShingle |
Heart hypoplasia in an animal model of congenital diaphragmatic hernia Tannuri,Uenis Congenital diaphragmatic hernia Heart Hypoplasia Fetus |
title_short |
Heart hypoplasia in an animal model of congenital diaphragmatic hernia |
title_full |
Heart hypoplasia in an animal model of congenital diaphragmatic hernia |
title_fullStr |
Heart hypoplasia in an animal model of congenital diaphragmatic hernia |
title_full_unstemmed |
Heart hypoplasia in an animal model of congenital diaphragmatic hernia |
title_sort |
Heart hypoplasia in an animal model of congenital diaphragmatic hernia |
author |
Tannuri,Uenis |
author_facet |
Tannuri,Uenis |
author_role |
author |
dc.contributor.author.fl_str_mv |
Tannuri,Uenis |
dc.subject.por.fl_str_mv |
Congenital diaphragmatic hernia Heart Hypoplasia Fetus |
topic |
Congenital diaphragmatic hernia Heart Hypoplasia Fetus |
description |
PURPOSE: In previous papers, we described a new experimental model of congenital diaphragmatic hernia in rabbits, and we also reported noninvasive therapeutic strategies for prevention of the functional and structural immaturity of the lungs associated with this defect. In addition to lung hypoplasia, pulmonary hypertension, biochemical, and structural immaturity of the lungs, the hemodynamics of infants and animals with congenital diaphragmatic hernia are markedly altered. Hence, cardiac hypoplasia has been implicated as a possible cause of death in patients with congenital diaphragmatic hernia, and it is hypothesized to be a probable consequence of fetal mediastinal compression by the herniated viscera. Cardiac hypoplasia has also been reported in lamb and rat models of congenital diaphragmatic hernia. The purpose of the present experiment was to verify the occurrence of heart hypoplasia in our new model of surgically produced congenital diaphragmatic hernia in fetal rabbits. METHODS: Twelve pregnant New Zealand rabbits underwent surgery on gestational day 24 or 25 (normal full gestational time - 31 to 32 days) to create left-sided diaphragmatic hernias in 1 or 2 fetuses per each doe. On gestational day 30, all does again underwent surgery, and the delivered fetuses were weighed and divided into 2 groups: control (non-surgically treated fetuses) (n = 12) and congenital diaphragmatic hernia (n = 9). The hearts were collected, weighed, and submitted for histologic and histomorphometric studies. RESULTS: During necropsy, it was noted that in all congenital diaphragmatic hernia fetuses, the left lobe of the liver herniated throughout the surgically created defect and occupied the left side of the thorax, with the deviation of the heart to the right side, compressing the left lung; consequently, this lung was smaller than the right one. The body weights of the animals were not altered by congenital diaphragmatic hernia, but heart weights were decreased in comparison to control fetuses. The histomorphometric analysis demonstrated that congenital diaphragmatic hernia promoted a significant decrease in the ventricular wall thickness and an increase in the interventricular septum thickness. CONCLUSION: Heart hypoplasia occurs in a rabbit experimental model of congenital diaphragmatic hernia. This model may be utilized for investigations in therapeutic strategies that aim towards the prevention or the treatment of heart hypoplasia caused by congenital diaphragmatic hernia. |
publishDate |
2001 |
dc.date.none.fl_str_mv |
2001-12-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0041-87812001000600003 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0041-87812001000600003 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/S0041-87812001000600003 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Faculdade de Medicina / Universidade de São Paulo - FM/USP |
publisher.none.fl_str_mv |
Faculdade de Medicina / Universidade de São Paulo - FM/USP |
dc.source.none.fl_str_mv |
Revista do Hospital das Clínicas v.56 n.6 2001 reponame:Revista do Hospital das Clínicas instname:Universidade de São Paulo (USP) instacron:USP |
instname_str |
Universidade de São Paulo (USP) |
instacron_str |
USP |
institution |
USP |
reponame_str |
Revista do Hospital das Clínicas |
collection |
Revista do Hospital das Clínicas |
repository.name.fl_str_mv |
Revista do Hospital das Clínicas - Universidade de São Paulo (USP) |
repository.mail.fl_str_mv |
||revista.hc@hcnet.usp.br |
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1754820894422728704 |