2014
DOI: 10.1016/j.placenta.2014.04.007
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Effect of maternal nutrient restriction and melatonin supplementation from mid to late gestation on vascular reactivity of maternal and fetal placental arteries

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Cited by 24 publications
(17 citation statements)
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“…Prevention of vascular dysfunction and microvascular rarefaction in rat offspring in a model of maternal protein restriction was also induced by antenatal treatment with the antioxidant Lazaroid (Cambonie et al, 2007). In an ovine model of nutrient restriction, pregnant ewes that were supplemented 5mg of melatonin had increased umbilical artery blood flow (Shukla et al, 2014). These studies all show proof of principle that antioxidant therapy can reverse deleterious phenotypes of developmental programming, however the doses used are far higher than used clinically and these studies focus on maternal supplementation, where in practice, phenotypes of developmental programming are more likely to be apparent at the time of or just after delivery, therefore postnatal antioxidant supplementation needs to be addressed.…”
Section: Intervention Strategiesmentioning
confidence: 99%
“…Prevention of vascular dysfunction and microvascular rarefaction in rat offspring in a model of maternal protein restriction was also induced by antenatal treatment with the antioxidant Lazaroid (Cambonie et al, 2007). In an ovine model of nutrient restriction, pregnant ewes that were supplemented 5mg of melatonin had increased umbilical artery blood flow (Shukla et al, 2014). These studies all show proof of principle that antioxidant therapy can reverse deleterious phenotypes of developmental programming, however the doses used are far higher than used clinically and these studies focus on maternal supplementation, where in practice, phenotypes of developmental programming are more likely to be apparent at the time of or just after delivery, therefore postnatal antioxidant supplementation needs to be addressed.…”
Section: Intervention Strategiesmentioning
confidence: 99%
“…However, the melatonin treatment during the pregnancy restores the placental efficiency at level of fetal body weight and fetal body/placental weight and induces the protein expression of Mn-SOD and catalase [ 59 ], suggesting that melatonin could be a candidate for protection/treatment of diseases characterized by placental ischemia such as intrauterine growth restriction, preeclampsia [ 73 ], or undernourished pregnancy [ 59 ]. Indeed, recent evidences have described that melatonin administration improved fetal-placental hemodynamic [ 74 ] and increased umbilical blood flow, an effect associated with “NO-dependent mechanisms” [ 75 ], as what occurs in cotyledonary placental arteries, via increased sensitivity to vasorelaxation agents such as bradykinin and lower contractile response to noradrenaline [ 76 ]. Additionally, melatonin administration reverted the increment of lipid peroxidation in the placenta and liver of mother and fetus exposed to cholestasis of pregnancy [ 77 ].…”
Section: Melatonin and The Placentamentioning
confidence: 99%
“…Umbilical arteries were dissected from the cords and cut into rings (2-3 mm) which were suspended in an organ bath containing Krebs solution bubbled with 95% O 2 5% CO 2 at 37 • C for isometric tension recording. The tissues were stretched to a resting tension of 2 g which was determined in preliminary experiments to be optimal based on the maximal response to 40 mM KCl [31]. After equilibration, rings were stimulated with 0.1 M U46619, in the absence or in the presence of N G -nitro-larginine methyl ester (l-NAME, 100 M), added 30 min before the addition of U46619, until they reached a steady-state contractile response and the flavonoids or vehicle (dimethylsulfoxide) were added to the chamber in a cumulative fashion.…”
Section: In Vitro Vascular Contractilitymentioning
confidence: 99%