The aim of the present study was to support the hypothesis that: 1) placental hypoperfusion is able to induce in intrauterine growth retarded (IUGR) fetuses metabolic adaptations leading to catabolism and 2) chronic hypoxia and substrate deprivation determine an increased production and release of ketone bodies from fetal side. To obtain a restriction in utero-placental blood flow seven pregnant rats were subjected to bilateral uterine artery ligationat 16 days' gestation pregnancy. Other six pregnant rats were submitted at sham operation. A third group of non manipulated rats served as controls for surgery and growing parameters. 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 samples were collected, from trunk and head after decapitation. As expected manipulated rats weight significantly lower than controls. A cetoacetate was significantly higher in IUGR fetuses of the ligated group than in sham operated fetuses (p <0.05). Moreover fetal ketone bodies levels of both study groups were higher than in their respective mothers. These findings confirm our hypothesis and provide evidence for fetal catabolism and endogenous ketogenesis in case of maternal placental hypoperfusion.
|Translated title of the contribution||Fetoneonatal metabolic adaptations after experimental placental hypoperfusion|
|Number of pages||5|
|Journal||Rivista Italiana di Pediatria|
|Publication status||Published - 1998|
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health