Document Detail

Fetal tracheal occlusion in the rat model of nitrofen-induced congenital diaphragmatic hernia: tracheal occlusion reverses the arterial structural abnormality.
MedLine Citation:
PMID:  11381408     Owner:  NLM     Status:  MEDLINE    
BACKGROUND/PURPOSE: The high mortality rate of congenital diaphragmatic hernia (CDH) is ascribed generally to pulmonary hypoplasia and persistent pulmonary hypertension characterized by associated pulmonary arterial structural changes. Prenatal tracheal occlusion (TO) accelerates lung growth, but the effect of TO on pulmonary arterial structure in CDH has not been well defined. The authors hypothesized that TO could reverse the pulmonary arterial structural changes observed in CDH. To address this hypothesis, we utilized the nitrofen-induced rat model of CDH to examine the effect of TO on pulmonary arterial morphology of CDH lungs. METHODS: Left-sided CDH was induced by administering 100 mg of nitrofen to pregnant Sprague-Dawley rats on day 9 of gestation. TO was performed on day 19, and the fetuses were harvested on day 21.5 of gestation. After the ductus arteriosus was ligated, the pulmonary arteries were injected with a barium-gelatin mixture, and the lungs were inflation fixed. Coronal sections of the lungs were stained with elastin van Gieson. External diameter (ED), internal diameter (ID), and medial and adventitial wall thickness of the pulmonary arteries were measured using a computer image analyzer, and the percent medial thickness (%MT) and adventitial thickness (%AT) were calculated. The lungs from nitrofen-exposed fetuses with left-sided CDH (CDH group), trachea-occluded left-sided CDH (CDH+TO group), non-CDH (non-CDH group), and normal fetuses (normal group) were compared. RESULTS: The %MT was significantly increased in all sizes of arteries in CDH compared with non-CDH and normal groups (P < .01). Compared with the CDH group, the CDH+TO group had significantly reduced %MT in all sizes of arteries (P < .01), to values comparable or less than the non-CDH and normal groups. The %AT of the CDH group was significantly increased in larger arteries compared with non-CDH and normal control groups (P < .01). CDH+TO had significantly decreased %AT compared with CDH in both larger (P < .01), and smaller arteries (P < .05) and that was comparable with the non-CDH and normal control groups. CONCLUSIONS: TO in hypoplastic CDH lung can reverse the pulmonary arterial structural changes that are seen in the nitrofen-induced fetal rat model of CDH. These data suggest that TO may reduce pulmonary vascular reactivity, and the risk of postnatal persistent pulmonary hypertension observed in human neonates with severe CDH. J Pediatr Surg 36:839-845.
M Kanai; Y Kitano; D von Allmen; P Davies; N S Adzick; A W Flake
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of pediatric surgery     Volume:  36     ISSN:  0022-3468     ISO Abbreviation:  J. Pediatr. Surg.     Publication Date:  2001 Jun 
Date Detail:
Created Date:  2001-05-30     Completed Date:  2001-08-02     Revised Date:  2003-11-14    
Medline Journal Info:
Nlm Unique ID:  0052631     Medline TA:  J Pediatr Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  839-45     Citation Subset:  IM    
Copyright Information:
Copyright 2001 by W.B. Saunders Company.
Children's Institute of Surgical Science and The Center for Fetal Diagnosis and Treatment, The Children's Hospital of Philadelphia, PA 19104-4399, USA.
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MeSH Terms
Analysis of Variance
Fetal Diseases / embryology,  pathology,  surgery*
Hernia, Diaphragmatic / congenital*,  embryology,  pathology,  surgery*
Lung / blood supply,  embryology,  pathology
Phenyl Ethers
Pulmonary Artery / abnormalities,  embryology*,  pathology
Rats, Sprague-Dawley
Trachea / embryology,  pathology,  surgery*
Reg. No./Substance:
0/Phenyl Ethers; 1836-75-5/nitrofen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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