Effects of acute asphyxia on brain energy metabolism in fetal guinea pigs near term.
In a previous study we suggested that--unlike other forms of asphyxia--acute asphyxia caused by arrest of uterine blood flow is accompanied by a fall in oxygen delivery to the fetal brain (Jensen et al., 1987). This may change cerebral energy metabolism by causing an increase in the glycolytic rate. To test this hypothesis we studied the time course of the changes in the levels of high-energy phosphates and glycolytic intermediates in the cerebral cortex of unanaesthetized fetal guinea pigs near term before and after 2 and 4 min of acute asphyxia. During asphyxia there was a progressive fall of adenosine triphosphate, creatine-phosphate, glucose and fructose-1,6-diphosphate concentrations, whereas adenosine diphosphate, adenosine monophosphate and lactate concentrations increased. Pyruvate concentrations did not change. We conclude that fetal cerebral energy metabolism becomes increasingly anaerobic during acute asphyxia caused by arrest of uterine blood flow, because oxygen delivery to the fetal brain falls.
Berger
R
R
Zentrum für Frauenheilkunde und Geburtshilfe der Justus-Liebig-Universität, Giessen, Germany.
Jensen
A
A
Krieglstein
J
J
Steigelmann
J P
JP
D000818:Animals; D001921:Brain / Q000378:metabolism*; D002540:Cerebral Cortex / Q000378:metabolism; D004734:Energy Metabolism; D005260:Female; D005311:Fetal Hypoxia / Q000378:metabolism*; D006019:Glycolysis; D006168:Guinea Pigs; D010710:Phosphates / Q000378:metabolism; D011247:Pregnancy; D014599:Uterus / Q000098:blood supply
D010710:Phosphates