The role of placental function in maintaining an adequate fetal growth has been addressed by many different laboratories. The relationship between maternal and fetal circulation in the placenta is crucial for efficient exchanges of oxygen and nutrients. Moreover, maturational changes are taking place throughout gestation within the placenta in order to increase the transfer capacities while fetal/placental weight ratio is significantly decreasing. In human pregnancies, an impairment in the invasion of fetal trophoblast cells into the maternal decidua has been hypothesized as a cause of placental insufficiency leading to intrauterine growth restriction (IUGR). This condition has been associated with a number of adaptive changes taking place in both placenta and fetus. Adaptive changes can be followed by pathology leading to fetal death and therefore staging of the disease is fundamental for timing of delivery.A classification of the severity of IUGR in human pregnancies has been proposed based upon fetal heart rate (FHR) and Doppler velocimetry of the umbilical artery (pulsatility index or PI). This classification of clinical severity reflects different degrees of placental insufficiency and is associated with significant differences in placental nutrient exchange. Only those IUGR with pathological PI and FHR are associated with increasing degrees of hypoxemia and lacticacidemia. Furthermore, significant differences are observed in the transplacental glucose gradient in the most severe cases and the placental transport of essential amino acids is significantly reduced both in vivo and in vitro. These findings suggest that both placental metabolism and transport are altered in intrauterine growth restriction in humans.
Copyright 2002 IFPA and Elsevier Science Ltd.