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A decrease in the PO2 of fetal arterial blood is observed in maternal alkalosis caused by hyperventilation in labour or exercise. The contribution of altered blood oxygen affinity to this effect was studied experimentally and by computer simulation of placental gas exchange. Thirteen guinea pigs near term of pregnancy were anesthetized and the right atrium of the fetus was catheterized to enable continuous and simultaneous measurement of PO2 and PCO2 by mass spectrometry. An infusion of base was given through a catheter in the descending aorta of the dam and the effect on fetal respiratory gas tensions observed. The mean change in maternal arterial pH measured in blood taken from a femoral artery was 0.07 +/- 0.04 (mean +/- S. D.). There was an immediate decrease in PO2 in the right atrium of the fetus, but no consistent alteration in PCO2. Two minutes after the start of the infusion, PO2 had fallen by 3.2 +/- 1.6 Torr (p less than 0.001) and PCO2 had risen by 1.7 +/- 1.8 Torr (not significant). The experiments were simulated using a mathematical model of placental gas exchange in the guinea pig. The model was able to predict the change in fetal arterial PO2, given numerical values for the pH, PO2 and PCO2 of fetal and maternal arterial blood prior to infusion of base and for maternal blood during the infusion of base. These values were obtained from the experimental data. Other input variables of the model were maternal and fetal hematocrit and DPG concentration, and the rates of blood flow on the two sides of the placenta.(ABSTRACT TRUNCATED AT 250 WORDS)

Contribution of the BOHR effect to the fall in fetal Po 2 caused by maternal alkalosis