Fetal and maternal endocrine changes during the induction of parturition with the PGF analogue, cloprostenol, in chronically catheterized sows and fetuses.
Parturition was induced in 8 catheterized sows 24-27 h after a single injection of the prostaglandin F (PGF) analogue, cloprostenol (200 micrograms, intramuscular), given at 105-106 days (4 sows) and 109-111 days (4 sows); term = 115 days. All catheterized fetuses were in good condition during the course of the induction and a normal percentage of live births occurred, although the subsequent viability of the piglets appeared to depend on the presence of an adequate suckling reflex. Maternal endocrine changes following cloprostenol included: (1) a rapid drop in plasma progesterone, which fell to below 5 ng/ml within 4 h, (2) a subsequent rise in 13, 14 dihydro-15-oxo prostaglandin F (PGFM) at about 6 h, with an increase in the venous-arterial difference across the uterus, (3) a large prepartum rise in PGFM from about 12 h, (4) a transient rise and fall in plasma cortisol immediately after the cloprostenol and a subsequent rise during labour, and (5) no detectable change in total unconjugated plasma oestrogen. During failed induction (2 sows) maternal progesterone levels remained above 5 ng/ml. In the fetuses, no changes in plasma progesterone were detectable following cloprostenol or during labour although there was a significant increase at birth. Fetal plasma cortisol concentrations had increased significantly 2 h after the cloprostenol, but a much greater cortisol surge began at 16-20 h reaching a maximum at birth. Fetal plasma oestrogen levels also increased just before delivery. These findings show that when farrowing is induced prematurely, the majority of the maternal endocrine changes are similar to those preceding spontaneous labour. However, the gradual rise in fetal plasma cortisol, which normally begins 4-6 days before term, is circumvented; instead a very rapid fetal cortisol surge begins after rather than before the drop in maternal progesterone and rise in PGFM. This results in high neonatal plasma cortisol levels in both catheterized and non-operated piglets and may well account for their viability.
D000818:Animals; D002404:Catheterization / Q000379:methods; D003008:Cloprostenol / Q000494:pharmacology*; D015237:Dinoprost / Q000031:analogs & derivatives*; D004967:Estrogens / Q000097:blood; D005260:Female; D005312:Fetal Blood / Q000187:drug effects; D005333:Fetus / Q000502:physiology; D006854:Hydrocortisone / Q000097:blood; D007751:Labor, Induced; D010913:Pituitary-Adrenal System / Q000187:drug effects* / Q000502:physiology; D011247:Pregnancy; D011374:Progesterone / Q000097:blood; D011460:Prostaglandins F / Q000097:blood; D011461:Prostaglandins F, Synthetic / Q000494:pharmacology*; D013552:Swine; D014599:Uterus / Q000187:drug effects / Q000502:physiology
D004967:Estrogens; D011460:Prostaglandins F; D011461:Prostaglandins F, Synthetic; C008228:15-keto-13,14-dihydroprostaglandin F2alpha; D003008:Cloprostenol; D011374:Progesterone; D015237:Dinoprost; D006854:Hydrocortisone