Development of cardiovascular function in the horse fetus.
In mammals, the mechanisms regulating an increase in fetal arterial blood pressure with advancing gestational age remain unidentified. In all species studied to date, the prepartum increase in fetal plasma cortisol has an important role in the maturation of physiological systems essential for neonatal survival. In the horse, the prepartum elevation in fetal cortisol and arterial blood pressure are delayed relative to other species. Hence, the mechanisms governing the ontogenic increase in arterial blood pressure in the horse fetus may mature much closer to term than in other fetal animals. In the chronically instrumented pony mare and fetus, this study investigated how changes in fetal peripheral vascular resistance, in plasma concentrations of noradrenaline, adrenaline and vasopressin, and in the maternal-to-fetal plasma concentration gradient of oxygen and glucose relate to the ontogenic changes in fetal arterial blood pressure and fetal plasma cortisol concentration as term approaches. The data show that, towards term in the horse fetus, the increase in arterial blood pressure occurs together with reductions in metatarsal vascular resistance, elevations in plasma concentrations of cortisol, vasopressin, adrenaline and noradrenaline, and falls in the fetal : maternal ratio of blood P(a,O(2)) and glucose concentration. Correlation analysis revealed that arterial blood pressure was positively related with plasma concentrations of vasopressin and noradrenaline, but not adrenaline in the fetus, and inversely related to the fetal : maternal ratio of blood P(a,O(2)), but not glucose, concentration. This suggests that increasing vasopressinergic and noradrenergic influences as well as changes in oxygen availability to the fetus and uteroplacental tissues may contribute to the ontogenic increase in fetal arterial blood pressure towards term in the horse.
Giussani
Dino A
DA
Department of Physiology, University of Cambridge, Cambridge CB2 3EG, UK. dag26@cam.ac.uk
Forhead
Alison J
AJ
Fowden
Abigail L
AL
D000818:Animals; D001786:Blood Glucose; D001794:Blood Pressure / Q000502:physiology*; D002319:Cardiovascular System / Q000196:embryology*; D004837:Epinephrine / Q000097:blood; D005260:Female; D005333:Fetus / Q000502:physiology*; D005865:Gestational Age; D006728:Hormones / Q000097:blood*; D006736:Horses / Q000196:embryology*; D006854:Hydrocortisone / Q000097:blood; D009638:Norepinephrine / Q000097:blood; D010100:Oxygen / Q000097:blood; D011247:Pregnancy; D014655:Vascular Resistance / Q000502:physiology*; D014667:Vasopressins / Q000097:blood
D001786:Blood Glucose; D006728:Hormones; D014667:Vasopressins; D010100:Oxygen; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine