Uterine blood flow and birth weight are reduced and the risk of pre-eclampsia is increased in high-altitude pregnancies. Since IUGR and pre-eclampsia are associated with reduced invasion and remodelling of maternal spiral arteries we asked whether the terminal ends of uteroplacental arteries located at the maternal-foetal decidual interface evidenced less remodelling in 19 high (3100 m) compared with 13 moderate (1600 m) altitude placentae from normal pregnancies. Previous work has demonstrated marked villous angiogenesis in high altitude placentae. We asked whether such changes are compensatory for reduced modelling and/or whether they contribute to increased birth weight. Placentae were randomly sampled and examined with immunohistochemistry to evaluate vessel remodelling and foetal capillary density. The decidual ends of uteroplacental arteries were 8-fold more likely to be remodelled at 1600 vs. 3100 m (OR=8.1; CI 2.4, 27.0,P< 0.001). There were more than twice as many uteroplacental arteries observed in the high vs. moderate altitude placentae (OR=2.1; CI: 1.3, 3.5, P=0.006). Foetal capillary density was greater at 3100 vs. 1600 m (P< 0.001), but did not relate to remodelling nor to birth weight. In this in vivo model for chronic hypoxia, remodelling is reduced, and villous angiogenesis is not fully compensatory for reduced PO(2).
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http://dx.doi.org/10.1053/plac.2002.0899 | DOI Listing |
Front Physiol
December 2024
Division of Reproductive Sciences, Department of Obstetrics and Gynecology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
During pregnancy, marked changes in vasculature occur. The placenta is developed, and uteroplacental and fetoplacental circulations are established. These processes may be negatively affected by genetic anomalies, maternal environment (i.
View Article and Find Full Text PDFSci Rep
December 2024
Robinson Research Institute, School of Biomedicine, University of Adelaide, Adelaide, SA, Australia.
Studies in humans and rodents show exercise in pregnancy can modulate maternal blood pressure, vascular volume, and placental efficiency, but whether exercise affects early uteroplacental vascular adaptations is unknown. To investigate this, CBA/J female mice mated with BALB/c males to generate healthy uncomplicated pregnancies (BALB/c-mated) or mated with DBA/2J males to generate abortion-prone pregnancies (DBA/2J-mated), were subjected to treadmill exercise (5 days/week, 10 m/min, 30 min/day for 6 weeks before and throughout pregnancy), or remained sedentary. In uncomplicated pregnancies, exercise caused symmetric fetal growth restriction in fetuses evidenced by reductions in fetal weight, crown-to-rump length, abdominal girth and biparietal diameter.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
January 2025
Department of Biomedical Informatics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States.
Hypertensive disorders of pregnancy represent an escalating global health concern with increasing incidence in low- to middle-income countries and high-income countries alike. The current lack of methods to detect the subclinical stages of preeclampsia (PE) and fetal growth restriction (FGR), two common vascular disorders of pregnancy, limits treatment options to minimize acute- and long-term adverse outcomes for both mother and child. To determine whether impaired maternal cardiovascular or uteroplacental vascular function precedes the onset of PE and/or FGR (PE-FGR), we used noninvasive techniques to obtain serial measurements of maternal cardiac output (CO), stroke volume (SV), systemic vascular resistance (SVR), and uterine and fetal arterial resistance at , -, and for 79 maternal-infant pairs in La Paz-El Alto, Bolivia (3,850 m), where the chronic hypoxia of high altitude increases the incidence of PE and FGR.
View Article and Find Full Text PDFClin Obstet Gynecol
December 2024
Division of Epidemiology and Biostatistics, Department of Obstetrics, Gynecology, and Reproductive Sciences.
Ischemic placental disease (IPD) is a constellation of obstetrical complications that include preeclampsia, placental abruption, and fetal growth restriction and affects 12% to 15% of pregnancies. The unifying pathophysiological mechanism that precedes all 3 complications is uteroplacental ischemia as a consequence of inadequate (or failure of) physiological transformation of the maternal uterine spiral arteries, endothelial cell dysfunction, and increased oxidative stress. This review summarizes the IPD literature, focusing on the epidemiology and risk factors, the effects of IPD on short and long-term maternal complications, and the association of IPD with perinatal, childhood, and long-term complications in offspring.
View Article and Find Full Text PDFJ Pers Med
November 2024
Department of Obstetrics and Gynecology, Faculty of Medicine, Karadeniz Technical University, 61080 Trabzon, Turkey.
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