AJP - Regulatory, Integrative and Comparative Physiology, Vol 261, Issue 5 1294-R1299, Copyright © 1991 by American Physiological Society
Is fetal acidosis in the human fetus maternogenic during labor? A reanalysis
F. Piquard, A. Schaefer, P. Dellenbach and P. Haberey
Department of Physiology, Faculty of Medicine, Louis Pasteur University, Strasbourg, France.
The purpose of this study was to investigate whether maternogenic fetal
acidosis can occur at the time of labor and delivery and to evaluate the
extent of the possible maternal contribution to fetal acidosis. We have
therefore determined fetal and maternal lactate concentrations and
acid-base status under various conditions in 589 women at the end of
gestation and during labor. The results show that metabolic acidosis
develops in all fetuses because of increased production of lactic acidosis
is primarily of fetal origin: 1) the umbilical arteriovenous lactate
differences were positive and large in steady-state conditions as well as
in depressed newborns; 2) the conditions that could produce a net transfer
of lactate from the mother to the fetus, namely a positive maternofetal
gradient of lactate and proton, were rarely observed; and 3) the
correlation between fetal and maternal lactate levels was very weak, with
regression coefficients decreasing from near steady-state conditions to
acute stress conditions, indicating that the increase in lactate in the
fetus and mother occurs independently. This correlation indicates also that
increased maternal lactate production under conditions of labor and
delivery can make a contribution by affecting the rate of net transfer from
fetus to mother. This is possible in approximately 6% of the fetuses.
