Loading…
Placental angiogenesis in sheep models of compromised pregnancy
Because the placenta is the organ that transports nutrients, respiratory gases and wastes between the maternal and fetal systems, development of its vascular beds is essential to normal placental function, and thus in supporting normal fetal growth. Compromised fetal growth and development have adve...
Saved in:
Published in: | The Journal of physiology 2005-05, Vol.565 (1), p.43-58 |
---|---|
Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Because the placenta is the organ that transports nutrients, respiratory gases and wastes between the maternal and fetal systems,
development of its vascular beds is essential to normal placental function, and thus in supporting normal fetal growth. Compromised
fetal growth and development have adverse health consequences during the neonatal period and throughout adult life. To establish
the role of placental angiogenesis in compromised pregnancies, we first evaluated the pattern of placental angiogenesis and
expression of angiogenic factors throughout normal pregnancy. In addition, we and others have established a variety of sheep
models to evaluate the effects on fetal growth of various factors including maternal nutrient excess or deprivation and specific
nutrients, maternal age, maternal and fetal genotype, increased numbers of fetuses, environmental thermal stress, and high
altitude (hypobaric) conditions. Although placental angiogenesis is altered in each of these models in which fetal growth
is adversely affected, the specific effect on placental angiogenesis depends on the type of âstressâ to which the pregnancy
is subjected, and also differs between the fetal and maternal systems and between genotypes. We believe that the models of
compromised pregnancy and the methods described in this review will enable us to develop a much better understanding of the
mechanisms responsible for alterations in placental vascular development. |
---|---|
ISSN: | 0022-3751 1469-7793 |
DOI: | 10.1113/jphysiol.2004.081745 |