Document Detail


The Endocrinology of equine parturition.
MedLine Citation:
PMID:  18704835     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Delivery of viable young requires co-ordination of fetal maturation with the onset of labour at term. In turn, this depends on a cascade of fetal and maternal endocrine events. The sequence of these events is broadly similar in most mammals but there are differences in placental hormone synthesis and in the timing and magnitude of key prepartum endocrine changes between species. In most farm animals, maternal progesterone (P4) levels decline and oestrogen levels increase in the last 5 - 10 days before delivery in response to activation of the fetal hypothalamicpituitary-adrenal (HPA) axis and increased fetal cortisol concentrations. This cortisol surge is also responsible for fetal maturation and increasing uteroplacental prostaglandin (PG) synthesis. In the mare, there is little, if any, P4 in the maternal plasma during late gestation and both progestagens and oestrogens are produced by a feto-placental unit which uses precursors supplied by the fetus to synthesise a range of C21 and C18 steroids, many of which are unique to the horse. Regulation of uterine quiescence and activation is, therefore, complex in the mare near term. Indeed, total progestagen concentrations rise and total oestrogen levels fall in the mare during the last 20 - 30 days of gestation and only show the changes typical of impending parturition in other species in the last 24 - 48 h before delivery. Fetal cortisol concentrations also rise late in gestation in the horse compared to other species. In common with other species, the prepartum endocrine cascade appears to begin in the fetal horse with activation of the fetal HPA axis but, initially, the primary product of the fetal equine adrenal appears to be pregnenolone (P5) and not cortisol. This leads to increased progestagen production by the uteroplacental tissues, which maintains uterine quiescence in the face of increasing uterine stretch caused by the rapidly growing fetus. Very close to term in association with increasing fetal ACTH levels, the fetal equine adrenals appear to switch to producing cortisol. This late cortisol surge induces a period of rapid fetal maturation and may also contribute to increased uteroplacental oestradiol-17 beta and PG production. The fall in P5 availability may reduce uteroplacental progestagen production and lift the block on myometrial contractility. Finally, increased PG secretion activates myometrial contractions, which stimulate oxytocin release via a neuroendocrine reflex. The endocrine regulation of equine parturition, therefore, involves progestagens, oestrogens, PGs and oxytocin as in other species. However, further studies are required to establish the causes and consequences of the rise and fall in maternal progestagens and the extent to which initiation of equine labour depends on the fetal HPA axis.
Authors:
A L Fowden; A J Forhead; J C Ousey
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association     Volume:  116     ISSN:  0947-7349     ISO Abbreviation:  Exp. Clin. Endocrinol. Diabetes     Publication Date:  2008 Jul 
Date Detail:
Created Date:  2008-09-03     Completed Date:  2008-11-18     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9505926     Medline TA:  Exp Clin Endocrinol Diabetes     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  393-403     Citation Subset:  IM    
Affiliation:
Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge. alf1000@cam.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Animals
Estrogens / physiology*
Female
Fetal Development / physiology
Horses / physiology*
Hypothalamo-Hypophyseal System / physiology
Parturition / physiology*
Pregnancy
Progestins / physiology*
Chemical
Reg. No./Substance:
0/Estrogens; 0/Progestins

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


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