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Publikationstyp: Zeitschriftenaufsatz
Dokumenttyp: Originalarbeit

Jahr: 2021

AutorInnen: Nagel, C; Aurich, C

Titel: Induction of parturition in horses - from physiological pathways to clinical applications.

Quelle: Domest Anim Endocrinol. 2021; 78:106670

Autor/innen der Vetmeduni Vienna:

Aurich Christine
Nagel Christina

Beteiligte Vetmed-Organisationseinheiten
Graf Lehndorff Institut für Pferdewissenschaften
Plattform Besamung und Embryotransfer

Based on the marked variability in physiological equine gestation length, induction of foaling in mares often results in the birth of dysmature foals. Precise prediction of preparedness of the mare for foaling is thus essential. Treatment with glucocorticoids mimics the fetal signal that initiates birth. Repeated daily dexamethasone treatment in late gestation results in birth of mature foals but the time from initiation of treatment to foaling is highly variable and complications such as dystocia have been reported. Contrary to most expectations, treatment of prepartum mares with progestogens does not delay but advances the onset of foaling. Prostaglandin F2α (PGF2α) and its analogues are effective to induce foaling but even in mares ready for parturition, foal health remains to some extent unpredictable. This may be caused by a relatively long interval between PGF2α treatment and birth, exposing the fetus for several hours to uterine contractions. Oxytocin reliably induces foaling towards the end of pregnancy, but when given at high doses is effective also in the pre-viable period of gestation, resulting in birth of premature foals. Recent research has focused on reducing the amount of oxytocin with the aim to induce foaling only in mares prepared for foaling. Mares selected on clinical criteria receive 1 dose of 2.5 to 3.5 IU of oxytocin. Mares not responding to oxytocin are judged not yet ready for foaling and treatment is repeated the earliest after 24 h. This protocol at present is the most reliable and safest way to induce parturition in mares.Copyright © 2021. Published by Elsevier Inc.

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