title: Postnatal cardiovascular function after manipulation of fetal growth by embryo transfer in the horse.
abstract: This study used between-breed embryo transfer in the horse to investigate the effects of maternal size and uterine capacity on fetal growth and postnatal cardiovascular and neuroendocrine functions. Equine embryos were transferred to establish eight Thoroughbred-in-Thoroughbred (TinT), seven Pony-in-Pony (PinP), five Thoroughbred-in-Pony (TinP) and eight Pony-in-Thoroughbred (PinT), pregnancies. Maternal and foal weights and placental microscopic area were measured at birth. At 6 days of postnatal life, arterial blood pressure and heart rate were monitored and blood samples were taken for hormone analysis before, during and after a 10 min period of nitroprusside-induced hypotension. Values for maternal and foal weights and placental area at birth were larger in TinT than in PinP pregnancies (P < 0.05). PinT pregnancies resulted in larger placentae and heavier foals relative to PinP (P < 0.05). TinP had smaller placentae and lighter foals relative to TinT (P < 0.05). Growth-enhanced (PinT) foals showed elevated basal arterial blood pressure and baroreflex threshold, reduced baroreflex sensitivity, diminished plasma catecholamine responses to acute stress, and increased cortisol responsiveness to ACTH. Conversely, growth-restricted (TinP) foals showed no change in basal arterial blood pressure, baroreflex threshold or adrenocortical responsiveness to ACTH, but had enhanced baroreflex sensitivity and augmented plasma catecholamine responses to acute stress. The data show that fetal growth acceleration as well as fetal growth restriction, resulting from between-breed embryo transfer in the horse, leads to altered postnatal regulation of blood pressure and the circulating concentrations of cortisol. These findings suggest that deviations in the pattern and rate of fetal growth both above and below the normal trajectory may influence cardiovascular function in postnatal life.
authors.affiliation: Department of Physiology and Clinical Veterinary Medicine, University of Cambridge, Cambridge CB2 3EG, UK. dag26@cam.ac.uk
authors.forename: Dino A
authors.initials: DA
authors.lastname: Giussani
authors.forename: Alison J
authors.initials: AJ
authors.lastname: Forhead
authors.forename: David S
authors.initials: DS
authors.lastname: Gardner
authors.forename: Andrew J W
authors.initials: AJ
authors.lastname: Fletcher
authors.forename: W R
authors.initials: WR
authors.lastname: Allen
authors.forename: Abigail L
authors.initials: AL
authors.lastname: Fowden
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D000831:Animals, Newborn; D017704:Baroreflex / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D001824:Body Constitution / Q000502:physiology; D002320:Cardiovascular Physiological Phenomena; D004624:Embryo Transfer / Q000662:veterinary*; D005314:Embryonic and Fetal Development / Q000502:physiology*; D004837:Epinephrine / Q000097:blood; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006736:Horses; D006854:Hydrocortisone / Q000097:blood; D007022:Hypotension / Q000139:chemically induced / Q000503:physiopathology; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology*; D009599:Nitroprusside; D009638:Norepinephrine / Q000097:blood; D011247:Pregnancy; D013045:Species Specificity; D014665:Vasodilator Agents
chemical_list: D014665:Vasodilator Agents; D009599:Nitroprusside; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine