Effects of placental pathology on maternal plasma progestagen and mammary secretion calcium concentrations and on neonatal adrenocortical function in the horse.
Between 1985 and 1990, 25 Thoroughbred mares were classified as having an abnormal pregnancy on the basis of precocious signs of impending parturition. Throughout the remainder of their pregnancies, plasma progestagen and mammary secretion calcium concentrations were monitored. After parturition, evidence of placental pathology was recorded and their foals were assessed with regard to adrenocortical function and behaviour. Seven pony mares were used to establish a model of placental pathology and, following induced placental separation, were subjected to the same protocol. Control animals consisted of 35 Thoroughbred mares and 39 pony mares, all considered to have normal pregnancies. Of the 25 abnormal mares, 16 had precociously increased plasma progestagen concentrations, 17 had precociously increased mammary calcium concentrations and 24 had an abnormal placenta. Eighteen live foals resulted, of which 11 appeared abnormal on the basis of behaviour. Adrenocortical function was assessed in 13; 4 had normo- and 3 hypofunction and 6 were intermediate. These results were independent of gestational age at delivery. Of 13 foals examined for plasma progestagens, 7 had normal and 6 abnormal concentrations. Following placental separation in the pony mares, maternal plasma progestagen concentrations increased in 4 of the 7 mares within 4-11 days and in 1 after 42 days; there was placental pathology in 3 of these mares, 1 of which aborted at 287 days gestation. There was no increment in progestagens in the remaining 2 mares, which aborted at 240 days and 271 days. It was concluded that placental dysfunction may be diagnosed from early plasma progestagen increments prior to 308 days gestation; and that foals that survive birth in these circumstances may be physiologically immature but often have normal or intermediate adrenocortical function, irrespective of gestational age. This is in contrast to foals born prematurely without maternal plasma progestagen or mammary secretion calcium increments.
Rossdale
P D
PD
Beaufort Cottage Stables, Newmarket, Suffolk.
Ousey
J C
JC
Cottrill
C M
CM
Chavatte
P
P
Allen
W R
WR
McGladdery
A J
AJ
D000324:Adrenocorticotropic Hormone / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D002118:Calcium / Q000032:analysis; D005260:Female; D006734:Horse Diseases / Q000378:metabolism / Q000503:physiopathology*; D006736:Horses / Q000378:metabolism / Q000502:physiology; D008321:Mammary Glands, Animal / Q000502:physiology; D007752:Obstetric Labor, Premature / Q000378:metabolism / Q000662:veterinary*; D010920:Placenta / Q000473:pathology*; D011247:Pregnancy; D011256:Pregnancy Outcome; D011372:Progestins / Q000097:blood
D011372:Progestins; D000324:Adrenocorticotropic Hormone; D002118:Calcium