Betamethasone-mediated vascular dysfunction and changes in hematological profile in the ovine fetus

1 Laboratory for Pregnancy and Newborn Research, Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853; and 2 Fetal Health Research Group, Department of Obstetrics and Gynecology, St. Thomas' Hospital, London SE1 7EH, United Kingdom Glucocorticoid administration to fetal sheep induces a sustained systemic blood pressure rise and an associated increase in femoral vascular resistance. We utilized a small vessel myograph to compare isometric vascular responses of small femoral arterial branches from fetal sheep infused intravenously with either betamethasone or vehicle in vivo from 128 days gestation. Changes in hematological parameters were also determined. Betamethasone was infused for 48 h to produce fetal plasma betamethasone concentrations similar to those observed in human fetuses after maternal treatment with betamethasone to accelerate fetal lung maturation. When compared with vessels removed from vehicle-infused fetuses, vessels obtained from betamethasone-treated fetuses exhibited 1 ) enhanced sensitivity to depolarizing potassium solutions; 2 ) no differences in response to the thromboxane mimetic U-46619 or norepinephrine; and 3 ) differential responses to vasodilators, enhanced sensitivity to ACh, but decreased response to bradykinin and forskolin. In addition, erythrocyte and leukocyte counts were increased in betamethasone-infused fetuses. These observations indicate that multiple mechanisms operate to increase fetal vascular resistance during antenatal betamethasone exposure. glucocorticoids; antenatal; vascular resistance; blood pressure; blood cells