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Updated: Jun 27, 2026

A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
Published on: June 24, 2020
Mechanism(s) of in utero meconium passage
1Department of Obstetrics and Gynecology, Harbor-UCLA Medical Center, Torrance, CA 90502, USA.
Abstract:
To use sheep and rat models and demonstrate that stressors activate fetal glucocorticoid (GC) system, corticotrophin-releasing factor (CRF) system and cholinergic neurotransmitter system (ChNS) leading to propulsive colonic motility and in utero meconium passage. Immunohistochemical studies (IHS) were performed to localize GC-Receptors, CRF-receptors and key molecules of ChNS in sheep fetal distal colon. CRF expression in placenta and enteric endocrine cells in fetal rat system were examined and the effects of acute hypoxia on in utero meconium passage was tested. IHS confirmed localization and gestation dependent changes in GC-Rs, CRF-Rs and cholinergic markers in sheep fetal colon. Rat placenta and enteric endocrine cells express CRF and gastrointestinal tract express CRF-Rs. Hypoxia is a potent inducer of meconium passage in term fetal rats. Stress is a risk factor for in utero meconium passage and laboratory animal models can be used to develop pharmacotherapy to prevent stress-induced in utero meconium passage.
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