FETONEONATAL METABOLIC ADAPTATIONS AFTER EXPERIMENTAL PLACENTAL HYPOPERFUSION

The aim of the present study was to support the hypothesis that: 1) pl acental hypoperfusion is able to induce in intrauterine growth retarde d (IUGR) fetuses metabolic adaptations leading to catabolism and 2) ch ronic hypoxia and substrate deprivation determine an increased product ion and release of ketone bodies from fetal side. To obtain a restrict ion in utero-placental bloodflow seven pregnant rats were subjected to bilateral uterine artery ligation at 16 days' gestation pregnancy. Ot her six pregnant mts were submitted at sham operation. A third group o f non manipulated rats served as controls for surgery and growing para meters. On day 20 (term 21), at the time of sacrifice, fetal viability was verified, and placental and fetal weights were obtained Maternal blood samples were collected by intracardiac puncture. Fetal blood sam ples were collected from trunk and head after decapitation. As expecte d manipulated mts weight significantly lower than controls. Acetoaceta te was significantly higher in IUGR fetuses of the ligated group than in sham operated fetuses (p < 0.05). Moreover fetal ketone bodies leve ls of both study groups were higher than in their respective mothers. These findings confirm our hypothesis and provide evidence for fetal c atabolism and endogenous ketogenesis in case of maternal placental hyp operfusion.