Cited by 128Pregnancy and preeclampsia studiesBirth, Development, and HealthNeonatal Respiratory Health Research

Effects of fetal growth restriction on lung development before and after birth: A morphometric analysis

Maritz, G.S., Cock, M.L., Louey, S., Joyce, B.J., Albuquerque, C.A., Harding, R.·2001·Pediatric Pulmonology

Abstract

Our aim was to determine the effects of fetal growth restriction (FGR) during late gestation on the structure of the lungs in the fetus near term and at 8 weeks after birth. The studies were performed using two groups of pregnant sheep and their offspring. In both groups, FGR was induced by umbilico‐placental embolisation (UPE); for fetal studies, UPE was performed from 120 days of gestation until 140 days (term, ∼146 days), when fetuses were killed for tissue analysis. For postnatal studies, UPE continued from 120 days until delivery at term; postnatal lambs were killed at 8 weeks after birth for tissue analysis. UPE led to a thicker pulmonary blood‐air barrier at 140 days of gestation and this difference, which was due to a thickened basement membrane, was still present at 8 weeks after birth. At 8 weeks, we also observed a smaller number of alveoli per respiratory unit, thicker interalveolar septa, and a greater volume density of lung tissue in FGR lambs compared to controls. These changes would be expected to impair gas exchange and alter the mechanical properties of the lungs. Our data show that structural alterations in the lungs induced by placental insufficiency were more evident at 8 weeks of postnatal age than near term, indicating that the effects of FGR on the lung may become more serious with age and may affect respiratory health later in life. Pediatr Pulmonol. 2001; 32:201–210. © 2001 Wiley‐Liss, Inc.

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Crossref · 10.1002/ppul.1109

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  • A growth-restricted fetus has fewer insulin-producing beta cells and reduced vascularization in the pancreas, and compromised structure and maturation of the brain, lungs, and liver.

    “In addition, the pancreas has fewer insulin-producing beta cells and reduced vascularization (159, 340, 473), and the structure and maturation of the brain (142), lungs (358, 359, 424, 460) and liver (209, 474) are compromised.”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [358]

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Authors
Maritz, G. S., Cock, M. L., Louey, S., Joyce, B. J., Albuquerque, C. A., & Harding, R.
Affiliations
  • University of the Western Cape (ZA)
  • Monash University (AU)
Corresponding author
Maritz, G.S.
Venue
Pediatric Pulmonology
Publisher
Wiley
Published
2001-08-28
Volume
32
Issue
3
Pages
201-210
ISSN
  • 1099-0496 (ISSN-L)
  • 8755-6863
OpenAlex
W1995602286
Cited by
128
References
35
Citations by year
2026: 2 · 2025: 3 · 2024: 8 · 2023: 2 · 2022: 4 · 2021: 1 · 2020: 4 · 2019: 4 · 2018: 6 · 2017: 5 · 2016: 4 · 2015: 12 · 2014: 8 · 2013: 8 · 2012: 6
FWCI
3.91
Type
journal article
Language
en
Open access
closed
Locations
  • Pediatric Pulmonology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Neonatal Respiratory Health Research
Keywords
fetal growth restriction, lung development, placental insufficiency, basement membrane thickening, alveolar number, interalveolar septa, postnatal lung development, sheep model, respiratory health
MeSH terms
Animals, Animals, Newborn, Anthropometry, Female, Fetal Growth Retardation, Lung, Placental Insufficiency, Pregnancy, Pulmonary Alveoli, Sheep

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