Maternal respiratory alkalosis from hyperventilation before delivery has been associated with depression and acidosis of some newborn infants. In thesein uterostudies of 6 primate fetuses, acute maternal hyperventilation significantly increased both the maternal and the fetal pH and thus increased the oxygen affinities of maternal and fetal hemoglobins. In comparison with the control period, during hyperventilation 71 % more CO2was removed from the uterus and its contents. The average O2consumption by the uterus and placenta, 3.4 ml/min, and the fetus, 2.1 ml/min was unchanged during hyperventilation. Mean pO2in the umbilical vein during hyperventilation fell to 24.8 mm Hg and saturation to 65%, and umbilical blood flow increased from 40 to 45 ml/min. Average uterine blood flow decreased slightly during hyperventilation. During these same comparison periods, neither maternal and fetal heart rate nor arterial venous pressures changed significantly. Thus, although pO2and saturation in the umbilical and uterine venous blood decreased, the amount of oxygen delivered to each fetus remained relatively constant due in part to an increase in umbilical blood flow and to shifts in the oxygen dissociation curves of fetal and adult hemoglobins.