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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
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