Abstract
Antenatal corticosteroids are often administered to women at risk of preterm birth to accelerate fetal lung development; however, there is evidence that this treatment may adversely affect placental function in some fetuses. Our group has recently demonstrated that wave reflections in the umbilical artery (UA), measured using high-frequency ultrasound, are sensitive to placental vascular abnormalities. In the present study, we used this approach to investigate the effect of maternal administration of betamethasone, a clinically relevant corticosteroid, on the feto-placental vasculature of the mouse. Fetuses were assessed at embryonic day (E)15.5 and E17.5 in C57BL6/J mice. At both gestational ages, the UA diameter, UA blood flow, and the wave reflection coefficient were significantly elevated in the betamethasone-treated mice compared to vehicle-treated controls. These observations support the interpretation that placental vascular resistance dropped with betamethasone treatment to an extent that could not be explained by vasodilation of the UA alone. Consistent with clinical studies, the effect of betamethasone on UA end-diastolic velocity was heterogeneous. Our results suggest that UA wave reflections are more sensitive to acute changes in placental vascular resistance compared with the UA pulsatility index, and this technique may have clinical application to identify a favorable placental vascular response to fetal therapies such as antenatal corticosteroids, where the fetal heart rate is likely to vary.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 823-831 |
| Number of pages | 9 |
| Journal | Biology of Reproduction |
| Volume | 101 |
| Issue number | 4 |
| DOIs | |
| State | Published - Oct 25 2019 |
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Keywords
- corticosteroids
- mouse
- placenta
- ultrasound
- umbilical artery
- wave reflection
ASJC Scopus subject areas
- Reproductive Medicine
- Cell Biology
Cite this
Effect of maternal betamethasone administration on feto-placental vascular resistance in the mouse. / Cahill, Lindsay S.; Whitehead, Clare L.; Hobson, Sebastian R.; Stortz, Greg; Kingdom, John C.; Baschat, Ahmet; Murphy, Kellie E.; Serghides, Lena; Macgowan, Christopher K.; Sled, John G.
In: Biology of Reproduction, Vol. 101, No. 4, 25.10.2019, p. 823-831.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effect of maternal betamethasone administration on feto-placental vascular resistance in the mouse
AU - Cahill, Lindsay S.
AU - Whitehead, Clare L.
AU - Hobson, Sebastian R.
AU - Stortz, Greg
AU - Kingdom, John C.
AU - Baschat, Ahmet
AU - Murphy, Kellie E.
AU - Serghides, Lena
AU - Macgowan, Christopher K.
AU - Sled, John G.
PY - 2019/10/25
Y1 - 2019/10/25
N2 - Antenatal corticosteroids are often administered to women at risk of preterm birth to accelerate fetal lung development; however, there is evidence that this treatment may adversely affect placental function in some fetuses. Our group has recently demonstrated that wave reflections in the umbilical artery (UA), measured using high-frequency ultrasound, are sensitive to placental vascular abnormalities. In the present study, we used this approach to investigate the effect of maternal administration of betamethasone, a clinically relevant corticosteroid, on the feto-placental vasculature of the mouse. Fetuses were assessed at embryonic day (E)15.5 and E17.5 in C57BL6/J mice. At both gestational ages, the UA diameter, UA blood flow, and the wave reflection coefficient were significantly elevated in the betamethasone-treated mice compared to vehicle-treated controls. These observations support the interpretation that placental vascular resistance dropped with betamethasone treatment to an extent that could not be explained by vasodilation of the UA alone. Consistent with clinical studies, the effect of betamethasone on UA end-diastolic velocity was heterogeneous. Our results suggest that UA wave reflections are more sensitive to acute changes in placental vascular resistance compared with the UA pulsatility index, and this technique may have clinical application to identify a favorable placental vascular response to fetal therapies such as antenatal corticosteroids, where the fetal heart rate is likely to vary.
AB - Antenatal corticosteroids are often administered to women at risk of preterm birth to accelerate fetal lung development; however, there is evidence that this treatment may adversely affect placental function in some fetuses. Our group has recently demonstrated that wave reflections in the umbilical artery (UA), measured using high-frequency ultrasound, are sensitive to placental vascular abnormalities. In the present study, we used this approach to investigate the effect of maternal administration of betamethasone, a clinically relevant corticosteroid, on the feto-placental vasculature of the mouse. Fetuses were assessed at embryonic day (E)15.5 and E17.5 in C57BL6/J mice. At both gestational ages, the UA diameter, UA blood flow, and the wave reflection coefficient were significantly elevated in the betamethasone-treated mice compared to vehicle-treated controls. These observations support the interpretation that placental vascular resistance dropped with betamethasone treatment to an extent that could not be explained by vasodilation of the UA alone. Consistent with clinical studies, the effect of betamethasone on UA end-diastolic velocity was heterogeneous. Our results suggest that UA wave reflections are more sensitive to acute changes in placental vascular resistance compared with the UA pulsatility index, and this technique may have clinical application to identify a favorable placental vascular response to fetal therapies such as antenatal corticosteroids, where the fetal heart rate is likely to vary.
KW - corticosteroids
KW - mouse
KW - placenta
KW - ultrasound
KW - umbilical artery
KW - wave reflection
UR - http://www.scopus.com/inward/record.url?scp=85075814610&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85075814610&partnerID=8YFLogxK
U2 - 10.1093/biolre/ioz128
DO - 10.1093/biolre/ioz128
M3 - Article
C2 - 31318405
AN - SCOPUS:85075814610
VL - 101
SP - 823
EP - 831
JO - Biology of Reproduction
JF - Biology of Reproduction
SN - 0006-3363
IS - 4
ER -