Umbilical and uteroplacental blood flow velocity waveforms in pregnancies with fetal growth retardation

1988 ◽  
Vol 27 (3) ◽  
pp. 187-196 ◽  
Author(s):  
Saemundur Gudmundsson ◽  
Karel Marsal
Keyword(s):  
Blood Flow ◽  
Flow Velocity ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Blood Flow Velocity ◽  
Fetal Growth Retardation ◽  
Uteroplacental Blood Flow

Working During Pregnancy: Effects on the Fetus

PEDIATRICS ◽  
1982 ◽  
Vol 69 (6) ◽  
pp. 724-727
Author(s):  
Richard L. Naeye ◽  
Ellen C. Peters
Keyword(s):  
Blood Flow ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Late Gestation ◽  
Fetal Growth Retardation ◽  
Maternal Factors ◽  
Third Trimester ◽  
The Third ◽  
Uteroplacental Blood Flow ◽  
Pregnancy Weight

In order to determine whether pregnancy outcome was altered when women were employed outside their homes, 7,722 pregnancies were analyzed. Gestations were not shortened but newborns of women who worked in the third trimester weighed 150 to 400 gm less than newborns of mothers who remained at home. The growth retardation was greatest when women were underweight pregravid and had a low pregnancy weight gain, when they were hypertensive, or when the work required standing. The growth retardation remained after the data were stratified by race, socioeconomic status, and other maternal factors that commonly influence fetal growth. The frequency of large placental infarcts progressively increased when women continued stand-up work into late gestation. Such infarcts reached a peak of 250/1,000 births after the 37th week of gestation in stand-up workers. Low uteroplacental blood flow is a likely explanation for both the fetal growth retardation and the large placental infarcts.

Role of leukocytes in uterine hypoperfusion and fetal growth retardation induced by ischemia-reperfusion

2001 ◽  
Vol 280 (3) ◽  
pp. H1215-H1221 ◽  
Author(s):  
Kei Miyakoshi ◽  
Hitoshi Ishimoto ◽  
Osamu Nishimura ◽  
Shinji Tanigaki ◽  
Mamoru Tanaka ◽  
...  
Keyword(s):  
Blood Flow ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Ischemia Reperfusion ◽  
Fetal Growth Retardation ◽  
Sprague Dawley ◽  
Pregnant Rats ◽  
Doppler Flowmetry ◽  
Leukocyte Accumulation ◽  
Sprague Dawley Rats

We investigated leukocyte involvement in uterine hypoperfusion and intrauterine fetal growth retardation (IUGR) induced by ischemia-reperfusion (I/R) in Sprague-Dawley rats. On day 17 of gestation, leukocyte accumulation in the uterus and placenta subjected to 30 min of ischemia, followed by reperfusion, was assessed by measuring myeloperoxidase (MPO) activity. Uterine MPO activity was significantly higher after 1 h of reperfusion than it was before ischemia ( P < 0.05), without any increase in placental MPO activity. Immunohistochemical staining showed leukocyte accumulation in the uterus subjected to I/R. The effects of treatment with monoclonal antibodies against CD11a (WT1) and CD18 (WT3) at a dose of 0.8 mg/kg on uterine blood flow and IUGR were investigated. Laser-Doppler flowmetry demonstrated that uterine hypoperfusion at 2 h after ischemia (blood flow, −51.7 ± 1.2%; P < 0.01) was inhibited by WT1 and WT3 treatment. I/R-induced IUGR at full term ( P < 0.05 vs. nonischemic horn) was prevented by WT1 and WT3 treatment on day 17. These results indicate that leukocyte accumulation may play an important role in the pathogenesis of uterine hypoperfusion and IUGR induced by I/R in pregnant rats.

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