THE PLACENTA IN INTRAUTERINE FETAL DEPRIVATION

Sixteen placentas from pregnancies complicated by mild preeclamptic toxemia, 11 placentas from pregnancies associated with severe pre‐eclampsia and intrauterine growth retardation (IGR), 14 placentas from IGR gestation of non‐toxemic origin, and 47 placentas from normal pregnancies terminated at 38–40 weeks by the birth of live babies, were investigated for total organ weight, DNA, protein content (PC), triglyceride (TG), cholesterol (CL), phospholipid phosphorus (P‐PL), percentage of dry matter, and for activity of enzymes with a regulatory function in the pathway of glycolysis, gluconeogenesis and NADPH generation. Feto/placental weight ratios and Apgar scores were also calculated. Placentas from pregnancies complicated by mild toxemia showed a significantly reduced proportion of dry matter, total DNA and PC. No significant changes in lipid content or enzyme activity were detected. The infants had normal birth weight and high Apgar scores. Placentas from pregnancies associated with severe pre‐eclamptic toxemia and IGR of non‐toxemic origin showed profound metabolic changes, not necessarily of the same nature. In placentas from severe toxemia, in addition to a decreased dry matter, DNA and PC, a significant increase in intracellular and whole placenta TG and P‐PL concentrations was observed as well as a decrease in CL/TG and CL/PL ratios. Concomitantly, the activity of pyruvate kinase (PK)—which regulates the energy generating glycolytic pathway at the cellular and whole placental levels—was decreased. The activity of enzymes that are connected with gluconeogenic and NADPH generating pathways, was also reduced when calculated per whole organ weight. These placental metabolic changes were accompanied by a significant reduction in placental and baby body weights and by decreased newborn Apgar scores. In contrast, in placentas from IGR pregnancies of non‐toxemic origin, the intracellular TG and PL contents were unchanged and whole placental concentrations were also decreased, despite a reduced DNA and whole placental PC. The CL/TG and CL/PL ratios also remained unchanged. PK activity proved significantly elevated at the cellular level and showed no changes when calculated per total placental weight. The same pattern was seen in the activity of enzymes related to NADPH generation whereas the activity of gluconeogenic enzymes was significantly decreased when calculated per whole placenta. On the basis of these results, it is suggested that IGR in severe toxemia may be closely connected with acceleration of the aging processes of placental tissue. On the other hand, in cases of IGR of non‐toxemic origin, the metabolic compensation at the cellular level in the small placenta facilitates adequate support for fetal growth. It therefore seems unlikely that in this group the IGR is of placental origin.