Cerebral oxidative metabolism during intrauterine growth retardation.
Cerebral oxidative metabolism during intrauterine growth retardation was investigated utilizing a pregnant-rat model. Dams were subjected to unilateral uterine artery ligation on the 17th day of gestation. At term, they were sacrificed by decapitation and the fetuses delivered by cesarean section. Body and brain weights of fetuses from ligated uterine segments were smaller than those of offspring from nonligated horns of the experimental rats or those from sham-operated dams. Blood glucose at birth was reduced by 25% in growth-retarded fetuses. Cerebral oxidative metabolites, including glycogen, glucose, lactate, ATP, and phosphocreatine, were not different from control levels. These findings suggest that neither tissue hypoxia nor deficient glucose delivery to brain can account for the stunted cerebral growth observed in fetuses following uterine artery ligation.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001835:Body Weight; D001921:Brain / Q000378:metabolism*; D005260:Female; D005317:Fetal Growth Retardation / Q000378:metabolism*; D005311:Fetal Hypoxia / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism; D007773:Lactates / Q000378:metabolism; D009929:Organ Size; D010101:Oxygen Consumption; D010725:Phosphocreatine / Q000378:metabolism; D011247:Pregnancy; D051381:Rats
D007773:Lactates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D006003:Glycogen; D005947:Glucose