Pontosubicular apoptosis (“necrosis”) in human neonates with intrauterine growth retardation and placental infarction

Burke, Christopher; Gobé, Glenda C.

doi:10.1007/s00428-005-1251-1

Cited by 29 publications

(16 citation statements)

References 23 publications

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“…During labor, uterine contractions can further compromise placental blood flow and oxygen supply to the FGR fetus, thereby increasing the risk of an intrapartum hypoxic-ischemic event and subsequent brain injury (9). Several authors have also reported that FGR fetuses are not only at great risk of perinatal hypoxic ischemic events but also may be more susceptible to hypoxic-ischemic brain damage, compared with appropriate-for-GA (AGA) fetuses (9,10).…”

Section: F Etal Growth Restriction (Fgr)mentioning

confidence: 99%

Carbohydrate and Energy Metabolism in the Brain of Rats With Thromboxane A2-Induced Fetal Growth Restriction

et al. 2011

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Fetal growth restriction (FGR) remains a cause of perinatal brain injury, sometimes leading to neurological and intellectual impairment. Although the mechanisms and pathophysiology of CNS injuries have not been elucidated completely, it is possible carbohydrate and energy metabolism may have an important role in the FGR brain. In this study, FGR was induced in rats by administration of synthetic thromboxane A 2 (STA 2 ). Pups were delivered by cesarean section. After killing, samples were obtained from the fetuses of both control and FGR rats for evaluation of carbohydrate and energy metabolism in brain tissue. Lactate and pyruvate levels in brain were reduced significantly in the FGR group. Glucose content in brain tissue tended to be increased in the FGR group. In contrast, glycogen content in brain tissue tended to be lower in the FGR group. However, these differences in glucose and glycogen content did not reach statistical significance. Brain high-energy reserves, including ATP, ADP, AMP, and phosphocreatine (P-Cr), were similar in the control and FGR groups. Gluconeogenesis compensated for chronic fetal hypoxia and decreased glycogen storage. Energy metabolism in the FGR brain is likely to be disrupted as a consequence of lower reserves of energy substrates. (Pediatr Res 70: 21-24, 2011) F etal growth restriction (FGR) is an important cause of perinatal morbidity and mortality. Surviving small-for-GA (SGA) infants have a higher incidence of neurological impairments including mental retardation and educational and/or behavioral problems (1-3). Several authors have reported that perinatal hypoxic ischemic brain damage may contribute to an increased prevalence of motor, cognitive, and affective disabilities in children born with FGR (4 -6). However, the mechanisms underlying these disabilities have not yet been fully elucidated.Various prenatal factors may affect fetal growth. Pregnancyinduced hypertension (PIH) is an especially important factor in FGR fetuses. In PIH, increasing umbilical vessel resistance causes limitations in uteroplacental blood flow. As a consequence, the supply of oxygen and nutrition to the fetus may decrease (7). FGR fetuses are frequently hypoxic and hypoglycemic (8). During labor, uterine contractions can further compromise placental blood flow and oxygen supply to the FGR fetus, thereby increasing the risk of an intrapartum hypoxic-ischemic event and subsequent brain injury (9). Several authors have also reported that FGR fetuses are not only at great risk of perinatal hypoxic ischemic events but also may be more susceptible to hypoxic-ischemic brain damage, compared with appropriate-for-GA (AGA) fetuses (9,10).Several studies have investigated the mechanisms of brain injuries in FGR model animals (11-13). Manipulations to induce FGR in animal models included surgical ligation of vessels supplying the uteroplacental unit (12) and maternal starvation (11). However, these models do not necessarily reflect the pathophysiology of FGR. It has been suggested that plasma levels ...

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Section: F Etal Growth Restriction (Fgr)mentioning

confidence: 99%

Carbohydrate and Energy Metabolism in the Brain of Rats With Thromboxane A2-Induced Fetal Growth Restriction

et al. 2011

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“…Large villous infarcts have been associated with ischemic CNS lesions in stillborns. 6,7 Finally, episodes of acute maternal hypotension related to cardiac arrest, amniotic fluid embolus, or septic shock are among the so-called ''sentinel events'' that can directly cause fetal brain injury.…”

Section: Maternal Circulatory Lesions Reduced Flow Large Vesselsmentioning

confidence: 99%

Disorders of Placental Circulation and the Fetal Brain

Redline¹

2009

Clinics in Perinatology

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“…(2009) 9 suggested that some placental abnormalities found were associated with clinical causes of still birth, such as placental infarction and IUGR. Burke C, Globe G (2005) 10 suggested that apoptosis was strongly associated with IUGR and placental infarction. Regarding calcification in IUGR group it was found in 6 placenta and in control group in 2 placenta.…”

Section: Study Group Control Groupmentioning

confidence: 99%

Histology of Placenta in Intrauterine Growth Restricted Pregnancy

Bal¹,

Basu²,

Bal³

2014

jemds

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INTRODUCTION:Placenta is found in all eutherian mammals. Study of placenta helps to gather information regarding the prenatal life of the fetus. Intrauterine growth restriction (IUGR) of the fetus occurs due to decreased supply of necessary elements to the fetus via the placenta and as a result some typical histological changes occur in placenta. AIMS AND OBJECTIVE: We wanted to study the histological features of placenta in IUGR pregnancy and to compare them with uncomplicated pregnancy. MATERIALS AND METHODS: In the Group A(study group)we had included 50 placentas from mother of IUGR babies with birth weight less than 10 th percentile of normal weight and in Group B(control group)there were 50 placentas from uncomplicated pregnancies. Placentas from mothers with IUGR due to congenital anomaly or infection were excluded. Tissues of placenta were taken and after preparation of slides different histological features like fibrin deposition, cytotrophoblastic hyperplasia, villous pattern, infarction, and calcification were noted. The two groups were compared statistically. RESULT ANALYSIS: In our study Risk ratio 1.36 indicates that in Study group A fibrin deposition was 1.36 times (36%) more than that of control group (risk ratio above or below 1 quantifies the relative increase or decrease in risk associated with).Syncytial knot formation were 1.05 times (5%) more in study group. Calcification 1.6 times (60%) and infarction 1.9 times (90%) higher in study group than control group. Significantly in placenta of study group Cytotrophoblastic hyperplasia (2.56 times more than control group), villous obliteration (3.57 times more than control group) and stromal fibrosis (2.33 times more than control group) were more than the control group. CONCLUSION: The present study depicted specific histological changes of placentas of IUGR pregnancy, thus explaining the role of examination of placenta to acquire knowledge about the prenatal life.

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Pontosubicular apoptosis (“necrosis”) in human neonates with intrauterine growth retardation and placental infarction

Cited by 29 publications

References 23 publications

Carbohydrate and Energy Metabolism in the Brain of Rats With Thromboxane A2-Induced Fetal Growth Restriction

Carbohydrate and Energy Metabolism in the Brain of Rats With Thromboxane A2-Induced Fetal Growth Restriction

Disorders of Placental Circulation and the Fetal Brain

Histology of Placenta in Intrauterine Growth Restricted Pregnancy

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