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

被引:55
作者
Anwar, MA
Schwab, M
Poston, L
Nathanielsz, PW
机构
[1] Cornell Univ, Coll Vet Med, Dept Biomed Sci, Lab Pregnancy & Newborn Res, Ithaca, NY 14853 USA
[2] St Thomas Hosp, Dept Obstet & Gynecol, Fetal Hlth Res Grp, London SE1 7EH, England
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 1999年 / 276卷 / 04期
关键词
glucocorticoids; antenatal; vascular resistance; blood pressure; blood cells;
D O I
10.1152/ajpheart.1999.276.4.H1137
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:H1137 / H1143
页数:7
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