Esophageal, tracheal and pulmonary parenchymal alterations in experimental esophageal atresia and tracheoesophageal fistula - A histological and morphometric study

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dc.contributor.authorOtcu, S
dc.contributor.authorKaya, M
dc.contributor.authorOzturk, H
dc.contributor.authorBuyukbayram, H
dc.contributor.authorDokucu, AI
dc.contributor.authorOnen, A
dc.contributor.authorYucesan, S
dc.date.accessioned2024-04-24T17:14:26Z
dc.date.available2024-04-24T17:14:26Z
dc.date.issued2002
dc.departmentDicle Üniversitesien_US
dc.description.abstractPulmonary complications are among the most important causes of morbidity and mortality in neonates with esophageal atresia and tracheofistula. We aimed to investigate the possible causes of respiratory complications encountered in esophageal atresia (EA) and tracheoesophageal fistula (TEF) in an experimental model. Sprague-Dawley fetal rats treated with adriamycin were used for the experiment. Time mated pregnant rats were given 1.75 mg/kg of adriamicyn intraperitoneally on days 6-9 of gestation. The fetuses were sacrified on day 21, weighed, and dissected under the surgical microscope. The animals were divided into four groups: (1) control group; (2) saline-injected group; (3) adriamycin-induced EA group, and (4) adriamycin administered but without development of EA. The lungs, esophagus, and trachea were excised and underwent histological examination. The mucosa of distal esophagus was thickened (p < 0.05); the submucosa was thinner (p < 0.05); and the muscular layer was thickened (p < 0.05) in fetuses with EA and TEF. In adriamycin-treated rats, in which EA and TEF developed, tracheal cartilage was loosened and formed into a D or C shape. The cartilage was fragmented into several segments on transverse sections in most fetuses. Alveolar septa were thin in lungs of fetus with EA and TEF (p < 0.05), without any fibrosis or evidence of parenchymal abnormality microscopically. Our findings suggest that respiratory complications may contribute to structural lesions in the trachea and particularly in the distal esophagus but not in the pulmonary parenchyma itself. Copyright (C) 2002 S. Karger AG, Basel.en_US
dc.identifier.doi10.1159/000065711
dc.identifier.endpage410en_US
dc.identifier.issn0014-312X
dc.identifier.issue6en_US
dc.identifier.pmid12403939
dc.identifier.scopus2-s2.0-0036971026
dc.identifier.scopusqualityQ2
dc.identifier.startpage405en_US
dc.identifier.urihttps://doi.org/10.1159/000065711
dc.identifier.urihttps://hdl.handle.net/11468/17938
dc.identifier.volume34en_US
dc.identifier.wosWOS:000179466500003
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherKargeren_US
dc.relation.ispartofEuropean Surgical Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectEsophageal Atresiaen_US
dc.subjectLung Developmenten_US
dc.subjectRespiratory Complicationen_US
dc.titleEsophageal, tracheal and pulmonary parenchymal alterations in experimental esophageal atresia and tracheoesophageal fistula - A histological and morphometric studyen_US
dc.titleEsophageal, tracheal and pulmonary parenchymal alterations in experimental esophageal atresia and tracheoesophageal fistula - A histological and morphometric study
dc.typeArticleen_US

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