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placental insufficiency/hypoxia
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Intrauterine growth restriction due to uteroplacental vascular insufficiency leads to increased hypoxia-induced cerebral apoptosis in newborn piglets.
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Uteroplacental vascular insufficiency in humans is a common cause of intrauterine growth restriction (IUGR) and is associated with an increased incidence of perinatal asphyxia and neurodevelopmental disorders compared to normal weight newborns. Experimental models that provide an opportunity to
Increased Umbilical Cord PAI-1 Levels in Placental Insufficiency Are Associated with Fetal Hypoxia and Angiogenesis.
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In intrauterine growth restriction (IUGR), a subset of pregnancies undergoes placental vascular dysregulation resulting in restricted blood flow and fetal hypoxemia. Altered transcription of hypoxic regulated plasminogen activator inhibitor 1 (PAI-1) has been associated with pregnancy complications
[Status and reaction to anoxia of rat fetuses developing in conditions of placental insufficiency].
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Significant adverse correlation of the fetus mass and the degree of its hydration was noted at term in rats with placental insufficiency induced by ligation of about 40% of preplacental vessels on the 16th day of gestation. Disorders revealed in transplacental water-salt metabolism are apparently of
Uteroplacental insufficiency lowers the threshold towards hypoxia-induced cerebral apoptosis in growth-retarded fetal rats.
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Infants suffering uteroplacental insufficiency and hypoxic ischemic injury often demonstrate cerebral apoptosis. Our objective was to determine the global effects of uteroplacental insufficiency upon cerebral gene expression of the apoptosis related proteins Bcl-2 and Bax and their role in
Fetal brain injury following prolonged hypoxemia and placental insufficiency: a review.
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It is well-established that severe, acute episodes of hypoxemia can damage the brain before birth, but the effects of more sustained hypoxemia are less well understood. We have used fetal fetal sheep in a series of studies aimed at determining the effects of prolonged hypoxemia, induced by placental
Hypoxia regulates insulin-like growth factor-binding protein 1 in human fetal hepatocytes in primary culture: suggestive molecular mechanisms for in utero fetal growth restriction caused by uteroplacental insufficiency.
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Intrauterine growth restriction (IUGR) can be a consequence of decreased uterine blood flow (uteroplacental insufficiency) and maternal and fetal hypoxia. Insulin-like growth factors (IGFs) and their binding proteins (IGFBPs) are key elements in fetal growth. IGF-I is a major growth promoter in
[Effect of acute "altitude" hypoxia on the transport function of the placenta of the rat with placental insufficiency and its correction using trental].
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Hypoxia or hyperoxia in placental insufficiency?
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Gender-specific differences in fetal cardiac troponin T in pregnancies complicated by placental insufficiency.
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BACKGROUND
Placental insufficiency and fetal growth restriction may lead to fetal hypoxia and acidemia, which result in fetal cardiac injury.
OBJECTIVE
The goal of this study was to compare the levels of fetal cardiac troponin T (cTnT) at birth and fetal Doppler parameters according to fetal gender
Brain allopregnanolone in the fetal and postnatal rat in response to uteroplacental insufficiency.
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OBJECTIVE
Allopregnanolone suppresses central nervous system activity and has neuroprotective actions in hypoxia-induced brain injury. In pregnant sheep allopregnanolone concentrations are high during fetal life and decline rapidly after birth. We investigated brain allopregnanolone concentrations
[Diagnosis and treatment of placental insufficiency in patients with congenital heart defects].
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The fetoplacental system was studied in 80 patients with congenital heart disease by placental scintigraphy, cardiotocography, and ultrasonic examination. Disordered uteroplacental blood flow was detected in 52 of the 64 patients, small-for-date fetuses in 36 of the 80, and chronic fetal hypoxia in
[What is the placental insufficiency syndrome?].
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The concept of "placental insufficiency" appears to offer a plausible explanation for foetal emergency situations; in reality, however, it leads to unproven and possibly wrong ideas on the genesis of these phenomena. It is applied in a semantically inconsistent manner, and that is one of the reasons
Epithelial membrane protein 2 (EMP2) deficiency alters placental angiogenesis, mimicking features of human placental insufficiency.
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Epithelial membrane protein-2 (EMP2) is a tetraspan protein predicted to regulate placental development. Highly expressed in secretory endometrium and trophectoderm cells, previous studies suggest that it may regulate implantation by orchestrating the surface expression of integrins and other
Nonresponsiveness of cerebral p53-MDM2 functional circuit in newborn rat pups rendered IUGR via uteroplacental insufficiency.
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Severe uteroplacental insufficiency causes cerebral apoptosis in the fetus. Moderate uteroplacental insufficiency causes intrauterine growth retardation (IUGR) and increases the risk of postnatal neurological morbidity. In the rat, uteroplacental insufficiency and IUGR affect cerebral gene
Reduced Perinatal Leptin Availability May Contribute to Adverse Metabolic Programming in a Rat Model of Uteroplacental Insufficiency.
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Leptin availability in perinatal life critically affects metabolic programming. We tested the hypothesis that uteroplacental insufficiency and intrauterine stress affect perinatal leptin availability in rat offspring. Pregnant rats underwent bilateral uterine vessel ligation (LIG; n = 14), sham
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