Placental Blood Flow and Fetal Oxygen Supply in Animal Models of Intra-Uterine Growth Retardation

Author(s):  
Anthony M. Carter
Reproduction ◽  
2017 ◽  
Vol 153 (3) ◽  
pp. R85-R96 ◽  
Author(s):  
E Mourier ◽  
A Tarrade ◽  
J Duan ◽  
C Richard ◽  
C Bertholdt ◽  
...  

In human obstetrics, placental vascularisation impairment is frequent as well as linked to severe pathological events (preeclampsia and intrauterine growth restriction), and there is a need for reliable methods allowing non-invasive evaluation of placental blood flow. Uteroplacental vascularisation is complex, and animal models are essential for the technical development and safety assessment of these imaging tools for human clinical use; however, these techniques can also be applied in the veterinary context. This paper reviews how ultrasound-based imaging methods such as 2D and 3D Doppler can provide valuable insight for the exploration of placental blood flow both in humans and animals and how new approaches such as the use of ultrasound contrast agents or ultrafast Doppler may allow to discriminate between maternal (non-pulsatile) and foetal (pulsatile) blood flow in the placenta. Finally, functional magnetic resonance imaging could also be used to evaluate placental blood flow, as indicated by studies in animal models, but its safety in human pregnancy still requires to be confirmed.


2016 ◽  
Vol 21 (32) ◽  
pp. 57-62
Author(s):  
Каркусова ◽  
Alla Karkusova ◽  
Бураева ◽  
Zarina Buraeva

Perinatal pathology, including congenital malformations of the fetus, is a serious problem of today’s society. The purpose of this study was to identify the significance of oligohydramnios in the diagnosis of congenital diseases in children. The study involved 140 pregnant women aged 18 to 42 years. It was found that while simultaneous revealing of oligohydramnios, fetal growth retardation, abnormal cardiotocography types, hemodynamic disturbances in the utero-placental blood flow risk of having children with congenital malformations is increased by 1.5 times. Thus, a more detailed search for the ultrasonic markers of congenital diseases, timely consulting of families in medical genetics facilities while oligohydramnios allows to prevent severe perinatal outcomes.


2003 ◽  
Vol 371 (1) ◽  
pp. 61-69 ◽  
Author(s):  
Maria L. LANGDOWN ◽  
Mark J. HOLNESS ◽  
Mary C. SUGDEN

Overexpression of the conserved Ca2+-binding proteins calreticulin and calsequestrin impairs cardiac function, leading to premature death. Calreticulin is vital for embryonic development, but also impairs glucocorticoid action. Glucocorticoid overexposure during late fetal life causes intra-uterine growth retardation and programmed hypertension in adulthood. To determine whether intra-uterine growth retardation or programmed hypertension was associated with altered calreticulin or calsequestrin expression, effects of prenatal glucocorticoid overexposure (maternal dexamethasone treatment on days 15—21 of pregnancy) were examined during fetal life and postnatal development until adulthood (24 weeks). Dexamethasone (100 or 200μg/kg of maternal body weight) was administered via osmotic pump. Calreticulin was detected as a 55kDa band and calsequestrin as 55 and 63kDa bands in 21 day fetal hearts. Only the 55kDa calsequestrin band was detected postnatally. Prenatal glucocorticoid overexposure at the higher dose decreased calreticulin protein expression (26%; P<0.05) but increased calsequestrin protein expression, both 55 and 63kDa bands, by 87% (P<0.01) and 78% (P<0.01); only the 55kDa calsequestrin band was increased at the lower dose (66%; P<0.05). Offspring of dams treated at the lower dexamethasone dose were studied further. In control offspring, cardiac calreticulin protein expression declined between 2 and 3 weeks of age, and remained suppressed until adulthood. Cardiac calsequestrin protein expression increased 2-fold between fetal day 21 and postnatal day 1 and continued to increase until adulthood, at which time it was 3.4-fold higher (P<0.001). Prenatal dexamethasone exposure minimally affected postnatal calsequestrin protein expression, but the postnatal decline in calreticulin protein expression was abrogated and calreticulin protein expression in adulthood was 2.2-fold increased (P<0.001) compared with adult controls. In view of the known associations between cardiac calreticulin overexpression and impaired cardiac function, targeted up-regulation of calreticulin may contribute to the increased risk of adult heart disease introduced as a result of prenatal overexposure to glucocorticoids.


2010 ◽  
Vol 36 (1) ◽  
pp. 58-63 ◽  
Author(s):  
V. Soubasi ◽  
S. Petridou ◽  
K. Sarafidis ◽  
Ch. Tsantali ◽  
E. Diamanti ◽  
...  

1978 ◽  
Vol 53 (1) ◽  
pp. 57-62 ◽  
Author(s):  
Lena Mårtensson ◽  
Per-Ove B. Sjöquist ◽  
Leif Bjellin ◽  
Anthony M. Carter

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