![]() The critical role of the placental blood supply is confirmed by the observation that intrauterine growth restriction (IUGR) in third-trimester human pregnancies is characterized by impaired uterine (maternal placental) and umbilical (fetal placental) blood flows, leading to reduced fetal nutrient uptake as well as fetal hypoxia, hypoglycaemia and asymmetric organ growth ( Pardi et al. 1985 Ferrell, 1991 Ferrell & Reynolds, 1992 Reynolds & Redmer,1995 Reynolds et al. 1975 Sreenan & Beehan, 1976 Knight et al. ![]() 1955 Hunter, 1956 Joubert & Hammond, 1958 Alexander, 1964 Alexander & Williams, 1971 Turman et al. 1942 Mckeown & Record, 1953 Eckstein et al. Thus, adequate blood flow to the placenta is critical for normal fetal growth, and it is not surprising that conditions that affect fetal growth, such as maternal and fetal genotype, increased numbers of fetuses, maternal nutrient excess or deprivation, environmental thermal stress, and high altitude (hypobaric) conditions, typically have similar effects on placental size, and also are associated with reduced rates of fetal oxygen and nutrient uptake, as well as reduced placental angiogenesis and blood flow ( Walton, 1938 Ebbs et al. ![]() ‘The fetal “lifeline” thus includes an adequate maternal placental circulation and supply of blood nutrients, a placenta that transports and metabolizes various substances properly and a functional fetal placental circulation.’ More recently, Lawrence Longo (1972) put a modern spin on this concept when he stated: (2005 b) for a brief review of this history). The importance of the placental circulation to fetal growth has been recognized since ancient times, as the above quotation from Aristotle makes abundantly clear (see Reynolds et al. ‘ The vessels join on the uterus like the roots of plants and through them the embryo receives its nourishment’.Īristotle, On the Generation of Animals (ca 340 bc). 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. 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 ‘stress’ to which the pregnancy is subjected, and also differs between the fetal and maternal systems and between genotypes. 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. 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. Compromised fetal growth and development have adverse health consequences during the neonatal period and throughout adult life. 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.
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