The DOI matches its Crossref record; 132 of the 132 references it cites were found in a registry or an index.
SHEEP MODELS OF INTRAUTERINE GROWTH RESTRICTION: FETAL ADAPTATIONS AND CONSEQUENCES
Abstract
SUMMARY: Intrauterine growth restriction (IUGR) has been associated with poor perinatal health outcomes. Animal models have been used to investigate why IUGR is associated with a poor prognosis. The sheep has been used extensively as an experimental model for IUGR with poor placental substrate supply to the fetus induced using a range of methods, including the surgical ablation of the majority of endometrial caruncles prior to conception, experimental induction of maternal hyperthermia, ligation of an umbilical artery or embolization of the placenta in late gestation and maternal overnutrition in the pregnant adolescent ewe. Fetal adaptations to fetal hypoxia and hypoglycaemia include activation of the fetal hypothalamic–pituitary–adrenal (HPA) axis and sympathetic nervous system and an associated increase in circulating cortisol and noradrenaline concentrations. Fetal cardiovascular responses vary according to the method used to induce placental dysfunction. Although an array of experimental models has been used to induce placental dysfunction at different stages of fetal development, each leads to remarkably similar fetal growth, metabolic, neuroendocrine and cardiovascular adaptations and consequences. The extent and range of the fetal physiological adaptations to chronic placental insufficiency are determined by the duration of exposure and the degree of the severity of substrate supply restriction. The present review summarizes how sheep models of IUGR have provided an increased understanding of the nature of the fetal adaptations to IUGR, their longer‐term physiological consequences and how to improve clinical management of IUGR in human pregnancies.
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“However, its strategy appears to differ with species, duration, severity and timing of the hypoxic insult, and/or the presence of fetal hypoxemia (393).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [393]
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Nutrition and brain development in early life
Prado, E. L., & Dewey, K. G. (2014) · Nutrition Reviews · doi:10.1111/nure.12102 · Cited by 1,036
Placental Origins of Chronic Disease
Burton, G. J., Fowden, A. L., & Thornburg, K. L. (2016) · Physiological Reviews · doi:10.1152/physrev.00029.2015 · Cited by 717
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Neonatal Morbidities of Fetal Growth Restriction: Pathophysiology and Impact
Malhotra, A., Allison, B. J., Castillo-Melendez, M., Jenkin, G., Polglase, G. R., & Miller, S. L. (2019) · Frontiers in Endocrinology · doi:10.3389/fendo.2019.00055 · Cited by 453
Metadata
- Authors
- Morrison, J. L.
- Affiliations
- University of South Australia (AU)
- Corresponding author
- Morrison, Janna L
- ORCID
- Morrison, Janna L
- Venue
- Clinical and Experimental Pharmacology and Physiology
- Publisher
- Wiley
- Published
- 2008-05-21
- Volume
- 35
- Issue
- 7
- Pages
- 730-743
- ISSN
- 0305-1870 (ISSN-L)
- 1440-1681
- OpenAlex
- W2054055548
- Cited by
- 289
- References
- 132
- Citations by year
- 2026: 8 · 2025: 19 · 2024: 15 · 2023: 21 · 2022: 14 · 2021: 24 · 2020: 24 · 2019: 11 · 2018: 24 · 2017: 16 · 2016: 22 · 2015: 20 · 2014: 8 · 2013: 16 · 2012: 16
- FWCI
- 1.54
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Clinical and Experimental Pharmacology and Physiology (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 › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Keywords
- fetal growth restriction, sheep model, placental insufficiency, fetal hypoxia, cortisol, norepinephrine, sympathetic nervous system, maternal hyperthermia, maternal overnutrition, fetal cardiovascular response, perinatal outcomes
- MeSH terms
- Adaptation, Physiological, Animals, Disease Models, Animal, Female, Fetal Growth Retardation, Humans, Placental Insufficiency, Pregnancy, Sheep, Overnutrition
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