Correlation Between Umbilical Arterial Flow and Placental Morphology

Kreczy, Alfons; Fusi, Luca; Wigglesworth, J. S.

doi:10.1097/00004347-199510000-00004

Cited by 19 publications

(7 citation statements)

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“…Altshuler [27] found increased perinatal mortality and congenital mal formations associated with chorangiosis. That a decrease in the number of small arteries may be associated with and contribute to growth retardation has been docu mented in recent clinical studies using Doppler [7,8,28], Rochelson et al [6] demonstrated abnormal flow by Doppler in trisomic placentas. Kreczy et al [28] corre lated abnormal umbilical arterial blood flow with a lower number of arteries in the tertiary stem villi, lower BW, and lower placental weight.…”

Section: Discussionmentioning

confidence: 95%

Trisomy 21 Placentas: Histopathological and Immunohistochemical Findings using Proliferating Cell Nuclear Antigen

Qureshi¹,

Jacques²,

Johnson³

et al. 1997

Fetal Diagn Ther

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Objective: The cause of growth retardation in trisomy 21 and other autosomal trisomies is not known, but may be the result of defective cell proliferation, slowing of the cell cycle, or placental structural abnormalities. Abnormalities of the fetal cell cycle may be reflected in placental growth and can be detected using proliferating cell nuclear antigen (PCNA). Methods: Twelve second-trimester and six third-trimester trisomy 21 placentas were examined histopathologically and stained immunohistochemically using antibodies to PCNA. Normal age-matched placentas were used as controls. Results: The second-trimester trisomy 21 placentas all exhibited many large irregular hypovascular villi. The third-trimester trisomy 21 placentas showed two patterns: (i) many large, irregular hypovascular villi, and (ii) relatively normal-appearing villi with only a few abnormal villi and focal hypervascularity. PCNA staining was significantly greater in second-trimester placentas when compared to third-trimester placentas for both trisomy 21 and controls. There was no significant difference in PCNA staining in trisomy 21 placentas when compared to the normal age-matched controls. Conclusions: PCNA staining indicates no significant differences in proliferation between normal and trisomy 21 placentas. Trisomy 21 placentas show villus abnormalities, including hypovascularity.

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Section: Discussionmentioning

confidence: 95%

Trisomy 21 Placentas: Histopathological and Immunohistochemical Findings using Proliferating Cell Nuclear Antigen

Qureshi¹,

Jacques²,

Johnson³

et al. 1997

Fetal Diagn Ther

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“…238 Elevated Doppler resistance indices in the maternal uterine arteries indicates there is downstream impedance to flow. This is accompanied by morphological evidence of placental structural problems such as a reduction in small arteries within the tertiatry stem villi, 239 thickening of the basal lamina and erythrocyte congestion in teriary villous capillaries 240,241 As with C a O 2 or P a O 2 , how one might target blood flow depends on what is the underlying problem. The vast majority of blood entering the intervillous space is carried by the maternal uterine arteries.…”

Section: Potential Drug Targets Of Important Placental Pathways Imentioning

confidence: 99%

Placental origins of adverse pregnancy outcomes: potential molecular targets: an Executive Workshop Summary of the Eunice Kennedy Shriver National Institute of Child Health and Human Development

Ilekis

Tsilou

Fisher

et al. 2016

American Journal of Obstetrics and Gynecology

231

167

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Although much progress is being made in understanding the molecular pathways in the placenta involved in the pathophysiology of pregnancy related disorders, a significant gap exists in utilizing this information for developing new drug therapies to improve pregnancy outcome. On March 5–6, 2015, the Eunice Kennedy Shriver National Institute of Child Health and Human Development of the National Institutes of Health sponsored a two day workshop titled Placental Origins of Adverse Pregnancy Outcomes: Potential Molecular Targets to begin to address this gap. Particular emphasis was given in the identification of important molecular pathways that could serve as drug targets and the advantages and disadvantages of targeting these particular pathways. This article is a summary of the proceedings of this workshop. A broad number of topics were covered ranging from basic placental biology to clinical trials. This included research in the basic biology of placentation, such as trophoblast migration and spiral artery remodeling, and trophoblast sensing and response to infectious and non-infectious agents. Research findings in these areas will be critical for formulating developing future treatments and developing therapies for the prevention of a number of pregnancy disorders of placental origin including preeclampsia, fetal growth restriction, and uterine inflammation. Research was also presented summarizing ongoing clinical efforts in the U.S. and in Europe testing novel interventions for preeclampsia and fetal growth restriction, including agents such as oral arginine supplementation, sildenafil, pravastatin, gene therapy using virally-delivered vascular endothelial growth factor, and oxygen supplementation therapy. Strategies were also proposed to improve fetal growth by enhancing nutrient transport to the fetus by modulating their placental transporters, as well as targeting placental mitochondrial dysfunction and oxidative stress to improve placental health. The roles of microRNAs and placental-derived exosomes, as well as messenger RNAs, were also discussed in the context of their use for diagnostics and as drug targets. The workshop discussed the aspect of safety and pharmacokinetic profiles of potential existing and new therapeutics that will need to be determined especially in the context of the unique pharmacokinetic properties of pregnancy, as well as the hurdles and pitfalls of translating research findings into practice. The workshop also discussed novel methods of drug delivery and targeting during pregnancy using macromolecular carriers, such as nanoparticles and biopolymers, to minimize placental drug transfer and hence fetal drug exposure. In closing, a major theme that developed from the workshop was that the scientific community needs to change their thinking of the pregnant women and her fetus as a vulnerable patient population for which drug development should be avoided, but rather thought of as a deprived population in need of more effective therapeutic interventions.

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“…At the level of the placenta, reduced uteroplacental perfusion leading to fetal hypoxia contributes to preeclampsia and/or fetal growth restriction (Aardema et al , 2001; Bower et al , 1993; Campbell et al , 1986; Konje et al , 2003; Lunell et al , 1984; Lunell et al , 1979; Zamudio et al , 1995), frequently associated with shallow or inadequate placentation (Brosens et al , 1972; Labarrere and Faulk, 1994; Meekins et al , 1994). Similarly, altered placental structure, diffusional distance or reduced fetoplacental perfusion have been associated with decreased oxygen transfer and reduced fetal growth (Aardema et al , 2001; Ferrazzi et al , 2000; Giles et al , 1986; Kreczy et al , 1995; Mayhew et al , 2004; Meekins et al , 1994; Todros et al , 1999). Although the relationship between hypoxia and decreased fetal growth is clear, the specific mechanism by which growth reduction takes place has not been described.…”

Section: Oxygen Hypoxia and Fetal Growthmentioning

confidence: 99%

Placental metabolic reprogramming: do changes in the mix of energy-generating substrates modulate fetal growth?

Illsley¹,

Caniggia²,

Zamudio³

2010

Int. J. Dev. Biol.

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Insufficient oxygen leads to the cessation of growth in favor of cellular survival. Our unique model of high-altitude human pregnancy indicates that hypoxia-induced reductions in fetal growth occur at higher levels of oxygen than previously described. Fetal PO2 is surprisingly high and fetal oxygen consumption unaffected by high altitude, whereas fetal glucose delivery and consumption decrease. Placental delivery of energy-generating substrates to the fetus is thus altered by mild hypoxia, resulting in maintained fetal oxygenation but a relative fetal hypoglycemia. Our data point to this altered mix of substrates as a potential initiating factor in reduced fetal growth, since oxygen delivery is adequate. These data support the existence, in the placenta, of metabolic reprogramming mechanisms, previously documented in tumor cells, whereby HIF-1 stimulates reductions in mitochondrial oxygen consumption at the cost of increased glucose consumption. Decreased oxygen consumption is not due to substrate (oxygen) limitation but rather results from active inhibition of mitochondrial oxygen utilization. We suggest that under hypoxic conditions, metabolic reprogramming in the placenta decreases mitochondrial oxygen consumption and increases anerobic glucose consumption, altering the mix of energy-generating substrates available for transfer to the fetus. Increased oxygen is available to support the fetus, but at the cost of less glucose availability, leading to a hypoglycemia-mediated decrease in fetal growth. Our data suggest that metabolic reprogramming may be an initiating step in the progression to more severe forms of fetal growth restriction and points to the placenta as the pivotal source of fetal programming in response to an adverse intrauterine environment.

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Correlation Between Umbilical Arterial Flow and Placental Morphology

Cited by 19 publications

References 0 publications

Trisomy 21 Placentas: Histopathological and Immunohistochemical Findings using Proliferating Cell Nuclear Antigen

Trisomy 21 Placentas: Histopathological and Immunohistochemical Findings using Proliferating Cell Nuclear Antigen

Placental origins of adverse pregnancy outcomes: potential molecular targets: an Executive Workshop Summary of the Eunice Kennedy Shriver National Institute of Child Health and Human Development

Placental metabolic reprogramming: do changes in the mix of energy-generating substrates modulate fetal growth?

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