ArticleReproductive sciences (Thousand Oaks, Calif.)2012
Impact of experimental diabetes on the maternal uterine vascular remodeling during rat pregnancy.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Hyperglycemia disturbs trophoblast functions and subsequently leads to failure of uterine spiral artery remodeling.Frontiers in endocrinology · 2023Review
- Modeling Trophoblast Cell-Guided Uterine Spiral Artery Transformation in the Rat.International journal of molecular sciences · 2022Review
- Impact of Immune Deficiency on Remodeling of Maternal Resistance Vasculature 4 Weeks Postpartum in Mice.Reproductive sciences (Thousand Oaks, Calif.) · 2017Article
- Immune Mechanisms Linking Obesity and Preeclampsia.Biomolecules · 2015Review
- Augmented dilation to nitric oxide in uterine arteries from rats with type 2 diabetes: implications for vascular adaptations to pregnancy.American journal of physiology. Heart and circulatory physiology · 2014Article
- Role of impaired endothelial cell Ca(2+) signaling in uteroplacental vascular dysfunction during diabetic rat pregnancy.American journal of physiology. Heart and circulatory physiology · 2013Article
- Inhibition of PPARγ during rat pregnancy causes intrauterine growth restriction and attenuation of uterine vasodilation.Frontiers in physiology · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Normal pregnancy is associated with an increase in uteroplacental blood flow in part due to growth and remodeling of the maternal uterine vasculature. In this study, we characterized the effect of diabetic pregnancy on vascular growth of the maternal uterine vasculature and on the passive mechanical properties of the uterine resistance arteries. Diabetes was induced in pregnant rats by injection of streptozotocin and confirmed by development of hyperglycemia. Fetuses of diabetic rats were significantly smaller and placentas larger compared to controls. Pregnancy-induced axial elongation of the mesometrial uterine vasculature was not altered by diabetes. Vascular wall thickness was unchanged between groups. Wall distensibility was increased and the rate constant of an exponential function fitted to stress-strain curve was significantly reduced demonstrating decreased wall stiffness in diabetic uterine radial arteries compared to controls. We conclude that experimental diabetes in rat pregnancy does not compromise the growth of maternal uterine vasculature but alters passive mechanical properties of the uterine radial arteries.
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Registered trials
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