Abstract:Placenta is an important organ that is crucial for both fetal and maternal health. Abnormalities of the placenta, such as during intrauterine growth restriction (IUGR) and pre-eclampsia (PE) are common, and an improved understanding of these diseases is needed to improve medical care. Biomechanics analysis of the placenta is an under-explored area of investigation, which has demonstrated usefulness in contributing to our understanding of the placenta physiology. In this review, we introduce fundamental biomech… Show more
“…The lowest levels of selenium were found in SGA neonates with maternal PIH ( p ≤ 0.001). PIH and SGA, because of intrauterine growth restriction, share similar pathophysiological features involving the placenta ( 69 ). PIH occurs because of shallow trophoblast invasion accompanied by inadequate remodeling of the spiral arteries, leading to placental insufficiency.…”
BackgroundPregnancy represents a state of increased oxidative stress and antioxidants, in which selenium (Se) plays a pivotal role, contribute to maintain the oxidative balance. If antioxidant defenses are depleted, placental function is disrupted, resulting in pregnancy complications, including pregnancy-induced hypertension (PIH). Little is known about fetal selenium status in concomitant relation to maternal PIH, gestational age (GA) and birthweight (BW).MethodsWe examined over a 3-year period the serum (SeS) and urine selenium (SeU) status in term neonates from normotensive (nonPIH) and hypertensive (PIH) mothers as clinical markers of oxidative stress. In this retrospective observational study, 72 neonates with maternal PIH were matched for GA and BW to 72 neonates of normotensive mothers. Four groups were obtained, based on maternal PIH and BW relative to GA (appropriate-for-gestational-age—AGA, small-for-gestational-age—SGA): nonPIH-AGA (control group), nonPIH-SGA, PIH-AGA, and PIH-SGA.ResultsThe results showed significant differences (p < 0.001) in selenium levels among the study groups: SeS - 44.85 ± 7.56 μg/L in nonPIH-AGA, 39.62 ± 11.42 μg/L in nonPIH-SGA, 40.01 ± 10.07 μg/L in PIH-AGA, and 25.39 ± 8.99 μg/L in PIH-SGA; SeU - 27.98 ± 7.99 μg/L in nonPIH-AGA, 22.85 ± 9.48 μg/L in nonPIH-SGA, 23.44 ± 6.73 μg/L in PIH-AGA, and 13.05 ± 5.86 μg/L in PIH-SGA. Selenium depletion was more common in neonates born from hypertensive mothers and those born small for gestational age. Though moderate in intensity, selenium levels were positively correlated with BW (0.319 for SeS, 0.397 for SeU) and negatively correlated with maternal systolic blood pressure (−0.313 for SeS, −0.324 for SeU). The main independent effects on SeS and SeU of each maternal blood pressure and birth weight turned out statistically significant. In interaction, a more pronounced effect was reached in PIH-SGA neonates.ConclusionSelenium status seemed to reflect the negative impact that PIH exerts in neonates during intrauterine development. Clinical markers of selenium status could thus be of great value for tracking responses of individuals to selenium supplementation as part of health improvement and harm mitigation approaches.
“…The lowest levels of selenium were found in SGA neonates with maternal PIH ( p ≤ 0.001). PIH and SGA, because of intrauterine growth restriction, share similar pathophysiological features involving the placenta ( 69 ). PIH occurs because of shallow trophoblast invasion accompanied by inadequate remodeling of the spiral arteries, leading to placental insufficiency.…”
BackgroundPregnancy represents a state of increased oxidative stress and antioxidants, in which selenium (Se) plays a pivotal role, contribute to maintain the oxidative balance. If antioxidant defenses are depleted, placental function is disrupted, resulting in pregnancy complications, including pregnancy-induced hypertension (PIH). Little is known about fetal selenium status in concomitant relation to maternal PIH, gestational age (GA) and birthweight (BW).MethodsWe examined over a 3-year period the serum (SeS) and urine selenium (SeU) status in term neonates from normotensive (nonPIH) and hypertensive (PIH) mothers as clinical markers of oxidative stress. In this retrospective observational study, 72 neonates with maternal PIH were matched for GA and BW to 72 neonates of normotensive mothers. Four groups were obtained, based on maternal PIH and BW relative to GA (appropriate-for-gestational-age—AGA, small-for-gestational-age—SGA): nonPIH-AGA (control group), nonPIH-SGA, PIH-AGA, and PIH-SGA.ResultsThe results showed significant differences (p < 0.001) in selenium levels among the study groups: SeS - 44.85 ± 7.56 μg/L in nonPIH-AGA, 39.62 ± 11.42 μg/L in nonPIH-SGA, 40.01 ± 10.07 μg/L in PIH-AGA, and 25.39 ± 8.99 μg/L in PIH-SGA; SeU - 27.98 ± 7.99 μg/L in nonPIH-AGA, 22.85 ± 9.48 μg/L in nonPIH-SGA, 23.44 ± 6.73 μg/L in PIH-AGA, and 13.05 ± 5.86 μg/L in PIH-SGA. Selenium depletion was more common in neonates born from hypertensive mothers and those born small for gestational age. Though moderate in intensity, selenium levels were positively correlated with BW (0.319 for SeS, 0.397 for SeU) and negatively correlated with maternal systolic blood pressure (−0.313 for SeS, −0.324 for SeU). The main independent effects on SeS and SeU of each maternal blood pressure and birth weight turned out statistically significant. In interaction, a more pronounced effect was reached in PIH-SGA neonates.ConclusionSelenium status seemed to reflect the negative impact that PIH exerts in neonates during intrauterine development. Clinical markers of selenium status could thus be of great value for tracking responses of individuals to selenium supplementation as part of health improvement and harm mitigation approaches.
“…The Navier-Stokes equation was utilised to characterise blood flow which considers the velocity vector, fluid pressure, density and viscosity. Two equations, one of continuity enforcing the principles of mass and momentum and a second which enforces Newton's second law, were also used [ 5 , 53 , 65 ].…”
Section: Umbilical Vessel and Chorionic Plate Modellingmentioning
confidence: 99%
“…Fetal development is entirely dependent on placental function. Any impairment can result in health implications which can extend into adulthood [ [3] , [4] , [5] ]. Fig.…”
“…The placenta is central to the pathogenesis of preeclampsia ( 19 ). Studies have revealed the altered feto-placental circulation in preeclampsia ( 20 ). NO is the most prominent vasodilator produced during pregnancy and plays a critical role in vasculogenesis and angiogenesis ( 21 ).…”
ObjectiveEndothelial functions in controlling blood flow in placental circulation are still unclear. The present study compares vascular dilations between placental circulation and other vessels, as well as between normal and preeclampsia placental vessels.MethodsPlacental, umbilical, and other vessels (cerebral and mesenteric arteries) were collected from humans, sheep, and rats. Vasodilation was tested by JZ101 and DMT. Q-PCR, Western blot, and Elisa were used for molecular experiments.ResultsEndothelium-dependent/derived vasodilators, including acetylcholine, bradykinin, prostacyclin, and histamine, mediated no or minimal dilation in placental circulation, which was different from that in other vessels in sheep and rats. There were lower mRNA expressions of muscarinic receptors, histamine receptors, bradykinin receptor 2, endothelial nitric oxide synthesis (eNOS), and less nitric oxide (NO) in human umbilical vessels when compared with placental vessels. Exogenous NO donors (sodium nitroprusside, SNP) and soluble guanylate cyclase (sGC) activators (Bay41-2272) decreased the baseline of vessel tone in placental circulation in humans, sheep, and rats, but not in other arteries. The sGC inhibitor ODQ suppressed the reduced baseline caused by the SNP. The decreased baseline by SNP or Bay41-2272 was higher in placental vessels than in umbilical vessels, suggesting that the role of NO/sGC is more important in the placenta. NO concentrations in preeclampsia placental vessels were lower than those in control, while no significant change was found in umbilical plasma between the two groups. eNOS expression was similar between normal and preeclampsia placental vessels, but phosphorylated eNOS levels were significantly lower in preeclampsia. Following serotonin, SNP or Bay41-2272-mediated dilations were weaker in preeclampsia placental vessels. The decreased amplitude of SNP- or Bay41-2272 at baseline was smaller in preeclampsia. The decreased amplitudes of ODQ + SNP were comparable between the two groups. Despite higher beta sGC expression, sGC activity in the preeclampsia placenta was lower.ConclusionThis study demonstrated that receptor-mediated endothelium-dependent dilation in placental circulation was significantly weaker than other vessels in various species. The results, showed firstly, that exogenous NO played a role in regulating the baseline tone of placental circulation via sGC. Lower NO production and decreased NO/sGC could be one of the reasons for preeclampsia. The findings contribute to understanding specific features of placental circulation and provide information about preeclampsia in placental vessels.
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