Umbilical vein blood flow in growth‐restricted fetuses

Ferrazzi, E.; Rigano, S.; Bozzo, Maddalena; Bellotti, M.; Giovannini, Niccolò; Galan, Henry L.; Battaglia, Frederick C.

doi:10.1046/j.1469-0705.2000.00208.x

Cited by 155 publications

(144 citation statements)

References 21 publications

(27 reference statements)

Supporting

Mentioning

132

Contrasting

Order By: Relevance

“…21,22 Reduced fetal growth in eNOS KO fetuses was associated with reduced umbilical blood flow per unit fetal weight, thus modeling human IUGR. 23 eNOS KO fetuses also exhibited fetal hypoxia, fetal erythrocyte immaturity, and reduced fetoplacental capillaries, thereby further mimicking IUGR in humans. 6,7,19,24 Interestingly, reduced NOS activity and expression occurs in subset of human IUGR placentas.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2013

View full text Add to dashboard Cite

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...

show abstract

Section: Discussionmentioning

confidence: 99%

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

et al. 2013

View full text Add to dashboard Cite

show abstract

“…Doppler ultrasound investigation of human FGR pregnancies exhibit increased impedance to umbilical arterial blood flows [75,76] and uterine blood flows [77,78]. Additionally, it has been shown during in vivo human study that the limitation in fetal oxygen delivery during FGR results from decreased placental transfer of oxygen as blood leaving the conceptus through the uterine veins has a higher PO 2 than control pregnancies and concomitantly, there is a lower uterine oxygen extraction rate [79].…”

Section: Placental Oxygen Transfer and Metabolismmentioning

confidence: 99%

The pregnant sheep as a model for human pregnancy

2008

View full text Add to dashboard Cite

Successful outcome of human pregnancy not only impacts the quality of infant life and well-being, but considerable evidence now suggests that what happens during fetal development may well impact health and well-being into adulthood. Consequently, a thorough understanding of the developmental events that occur between conception and delivery is needed. For obvious ethical reasons, many of the questions remaining about the progression of human pregnancy can not be answered directly, necessitating the use of appropriate animal models. A variety of animal models exist for the study of both normal and compromised pregnancies, including laboratory rodents, non-human primates and domestic ruminants. While all of these animal models have merit, most suffer from the inability to repetitively sample from both the maternal and fetal side of the placenta, limiting their usefulness in the study of placental or fetal physiology under non-stressed in vivo conditions. No animal model truly recapitulates human pregnancy, yet the pregnant sheep has been used extensively to investigate maternal-fetal interactions. This is due in part to the ability to surgically place and maintain catheters in both the maternal and fetal vasculature, allowing repeated sampling from non-anesthetized pregnancies. Considerable insight has been gained on placental oxygen and nutrient transfer and utilization from use of pregnant sheep. These findings were often confirmed in human pregnancies once appropriate technologies became available. The purpose of this review is to provide an overview of human and sheep pregnancy, with emphasis placed on placental development and function as an organ of nutrient transfer.

show abstract

“…Volume flow indices per unit of estimated fetal weight should therefore be interpreted with caution. 40 It has been hypothesized that an adverse fetal environment and subsequent reduced fetal growth result in fetal blood flow redistribution and permanent fetal cardiovascular changes, such as increased arterial wall stiffness and left ventricular dysfunction. 1,4,6,8 Studies in infants and adults have shown an association between small size at birth and increased arterial wall stiffness.…”

Section: Cardiac Circulationmentioning

confidence: 99%

Fetal Hemodynamic Adaptive Changes Related to Intrauterine Growth

Verburg¹,

Jaddoe²,

Wladimiroff³

et al. 2008

Circulation

134

131

View full text Add to dashboard Cite

Background-It has been suggested that an adverse fetal environment increases susceptibility to hypertension and cardiovascular disease in adult life. This increased risk may result from suboptimal development of the heart and main arteries in utero and from adaptive cardiovascular changes in conditions of reduced fetal growth. The aim of the present study was to evaluate whether reduced fetal growth is associated with fetal circulatory changes and cardiac dysfunction. Methods and Results-This study was embedded in a population-based, prospective cohort study starting in early fetal life.Fetal growth characteristics and fetal circulation variables were assessed with ultrasound and Doppler examinations in 1215 healthy women. The fetal circulation was examined in relation to estimated fetal weight. Higher placental resistance indices were strongly associated with decreased fetal growth. Cerebral resistance showed a gradual decline with reduced fetal growth. Cardiac output, peak systolic velocity of the outflow tracts, and cardiac compliance showed a gradual reduction with diminished fetal growth, whereas intraventricular pressure gradually increased. Conclusions-Decreased

show abstract

Umbilical vein blood flow in growth‐restricted fetuses

Abstract: The present study clearly establishes that umbilical venous blood flow is reduced in IUGR fetuses on a weight-specific basis. The sonographic growth parameter which best distinguishes umbilical flow differences of IUGR fetuses from normal fetuses is the head circumference.

Cited by 155 publications

References 21 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

The pregnant sheep as a model for human pregnancy

Fetal Hemodynamic Adaptive Changes Related to Intrauterine Growth

Contact Info

Product

Resources

About