Article

Mechanism(s) of in utero meconium passage

Department of Obstetrics and Gynecology, Harbor-UCLA Medical Center, Torrance, CA 90502, USA.
Journal of perinatology: official journal of the California Perinatal Association (Impact Factor: 2.07). 12/2008; 28 Suppl 3:S8-13. DOI: 10.1038/jp.2008.144
Source: PubMed

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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    • "By stimulating the cholinergic system and increasing colonic motility, CRF receptor 1 (CRF R1), a CRF-specific receptor subtype, is thought to be responsible for stress-induced dyspepsia and other complaints related to the gastrointestinal system[19,20]. Lakshmanan et al., studied the relationship between hypoxia and CRF with experiments conducted on mice[2]. In one such experiment , meconium was found in the amniotic fluid of fetal mice exposed to intrauterine hypoxia, whereas no meconium was detected in fetal mice in control groups that were not hypoxic[6]. "

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