Umbilical blood flow during pregnancy: evidence for decreasing placental perfusion

Link, G.; Clark, Kenneth E.; Lang, Uwe

doi:10.1016/j.ajog.2006.11.017

Cited by 40 publications

(37 citation statements)

References 23 publications

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“…During normal late gestational development in mice (current study), as in humans, 20 umbilical venous blood flow increased in association with an increase in umbilical vein diameter, whereas mean blood velocity remained constant. Also observed was a marked decrease in umbilical blood flow expressed per unit fetal weight with advancing gestation in mice (current study) as in humans.…”

Section: Discussionmentioning

confidence: 99%

“…Also observed was a marked decrease in umbilical blood flow expressed per unit fetal weight with advancing gestation in mice (current study) as in humans. 20 This was likely permitted by enhanced placental exchange efficiency as a result of the maturation and thinning of the placental barrier and by the increase in fetoplacental vascularity that is observed in late gestation in both species. 21,22 Reduced fetal growth in eNOS KO fetuses was associated with reduced umbilical blood flow per unit fetal weight, thus modeling human IUGR.…”

Section: Discussionmentioning

confidence: 99%

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Endothelial NO Synthase Augments Fetoplacental Blood Flow, Placental Vascularization, and Fetal Growth in Mice

et al. 2013

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Abstract-It is not known whether eNOS deficiency in the mother or the conceptus (ie, placenta and fetus) causes fetal growth restriction in mice lacking the endothelial NO synthase gene (eNOS knockout [KO]). We hypothesized that eNOS sustains fetal growth by maintaining low fetoplacental vascular tone and promoting fetoplacental vascularity and that this is a conceptus effect and is independent of maternal genotype. We found that eNOS deficiency blunted fetal growth, and blunted the normal increase in umbilical blood flow and umbilical venous diameter and the decrease in umbilical arterial Resistance Index in late gestation (14.5-17.5 days) in eNOS KO relative to C57Bl/6J controls. On day 17.5, fetoplacental capillary lobule length and capillary density in vascular corrosion casts were reduced in eNOS KO placentas. Reduced vascularization may be a result of decreased vascular endothelial growth factor mRNA and protein expression in eNOS KO placentas at this stage. These factors, combined with significant anemia found in eNOS KO fetuses, would be anticipated to reduce fetal oxygen delivery and contribute to the fetal tissue hypoxia that was detected in the heart, lung, kidney, and liver by immunohistochemistry using pimonidazole. Although maternal eNOS deficiency impairs uteroplacental adaptations to pregnancy, maternal genotype was not a significant factor affecting growth in heterozygous conceptuses. This indicates that fetal growth restriction was primarily caused by conceptus eNOS deficiency. In mice, placental hemodynamic and vascular changes with gestation and growth restriction showed strong parallels with human pregnancy. Thus, the eNOS KO model could provide insights into the pathogenesis of human intrauterine growth restriction. and vasculogenesis as shown in other vascular beds studied in adult animals. 13In the current study, we hypothesized that eNOS sustains fetal growth by maintaining low fetoplacental vascular tone and promoting fetoplacental vascularity. We further hypothesized that this is a conceptus effect and is independent of maternal genotype. We used eNOS knockout (KO) pregnancies because eNOS KO fetuses exhibit fetal growth restriction in late gestation, [14][15][16] and pregnant eNOS KO mothers exhibit impaired uteroplacental remodeling and a blunted rise in uteroplacental blood flow and cardiac output. 15,16 However, they neither overexpress sFlt1 mRNA in the placenta 16 nor do they become more hypertensive during pregnancy. [16][17][18] In this study, we quantified umbilical vein blood flow and umbilical artery Resistance Index using micro-ultrasound, visualized the fetoplacental vasculature using vascular corrosion casts, and evaluated hypoxia in the fetus in eNOS KO mice and in the background strain, C57Bl/6J (wild type [WT]). Whether IUGR is secondary to reduced uteroplacental perfusion or is a result of effects of eNOS deficiency in the conceptus in this model is not clear. Thus, crossbreeding experiments were performed to determine the impact of maternal genotype on the fetal phen...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Endothelial NO Synthase Augments Fetoplacental Blood Flow, Placental Vascularization, and Fetal Growth in Mice

et al. 2013

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“…Similar derangements can also occur in neonatal biochemistry leading to neonatal seizures. [8] It can also lead to uterine rupture if proper monitoring is not done. Another inducing agent misoprostol, prostaglandin E1 is less expensive, more stable and easier to store than PGE2.…”

Section: Introductionmentioning

confidence: 99%

Outcome of Induction of Labor: A Prospective Study

Lamichhane¹,

Subedi²,

Banerjee³

et al. 2016

AIMDR

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Background: Induction is defined as artificial initiation of uterine contraction with the aim of achieving the normal vaginal delivery. It is most widely accepted obstetrical intervention worldwide. The most common indication for induction is post dated pregnancy. Objective: To assess the outcome of induction in both mother and baby. Methods: During our study period, 391 patients were selected for induction due to various indications. Most of them were induced with tablet Misoprostol and only those with higher degree of gravida were induced with Dinoprostone gel intracervically and maternal and fetal outcome was seen.Results: Out of 4020 patients, induction rate was 9.72%. Among them 98.2% were induced with Misoprostol. Most of the induced age group was in between 20-30 years of age with primigravida 62%. Among them 48.59% were in between 40-41 weeks of gestation with 93% of having poor bishops score. About 67.7% had normal vaginal delivery with 4.86%, assisted with instrumental delivery. Cesarean section was seen in 32.3% of patients. Most common indications for LSCS were for failed induction (44%). Regarding the fetal outcome 99.7% born alive, 97.92% went to mother side, 2.07% admitted and 0.51% expired. Beside this, 88.7% had birth weight between 2.5 to 3.5 kg and 87.4% had clear liquor and 99.22% had the good apgar score. Conclusion: Though the cesarean section rate is higher in this study in comparison of WHO references to be not more than 15% but still the induction is beneficial in high-risk pregnancy where continuing the pregnancy is more hazardous than to termination.

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“…weight (Link et al, 2007). The aim of our study was to determine the degree of discordance of umbilical venous volume flow (UVVF), birthweight and placental share in MCs with and without sIUGR.…”

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confidence: 99%

The Relationships of Umbilical Venous Volume Flow, Birthweight and Placental Share in Monochorionic Twin Pregnancies With and Without Selective Intrauterine Growth Restriction

Chang¹,

Chang

Chao

et al. 2011

Twin Res Hum Genet

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This study was conducted to investigate the relationship among umbilical venous volume flow, birthweight and placental share in monochorionic twins with or without selective growth restriction. Having excluded cases complicated with twin-to-twin transfusion syndrome and one co-twin suffering intrauterine fetal death, a total of 51 monochorionic twin pregnancies were divided into two groups as with (group 1) and without (group 2) selective intrauterine growth restriction. Umbilical venous volume flow was calculated by multiplying the umbilical vein cross-sectional area by half of the maximal velocity around mid-trimester. The placentas were cut along the vascular equator into two individual placental masses. The discordance of birthweight was calculated as [(birthweight of larger twin—birthweight of smaller twin)/birthweight of larger twin 100%]. The discordances of umbilical venous volume flow and placental share were calculated in a similar fashion. The median umbilical venous volume flow discordances (68.4% and 15.3% in groups 1 and 2 monochorionic twins, respectively) were similar and correlated well with the placental share discordances (66.6% and 18.5% in groups 1 and 2 monochorionic twins, respectively) but not with the birthweight discordance (28.6% and 6.4% in groups 1 and 2 monochorionic twins, respectively) in both groups. We concluded that the umbilical venous volume flow discordance reflects the placental share discordance rather than the birthweight discordance in monochorionic twin pregnancies.

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Umbilical blood flow during pregnancy: evidence for decreasing placental perfusion

Cited by 40 publications

References 23 publications

Endothelial NO Synthase Augments Fetoplacental Blood Flow, Placental Vascularization, and Fetal Growth in Mice

Endothelial NO Synthase Augments Fetoplacental Blood Flow, Placental Vascularization, and Fetal Growth in Mice

Outcome of Induction of Labor: A Prospective Study

The Relationships of Umbilical Venous Volume Flow, Birthweight and Placental Share in Monochorionic Twin Pregnancies With and Without Selective Intrauterine Growth Restriction

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