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Maternal serum SP1 concentration was measured at 10-13 weeks' gestation in samples from 87 pregnancies with fetal chromosomal abnormalities (trisomy 21 n = 45; trisomy 18 n = 19; trisomy 13 n = 8; Turner syndrome n = 7; 47,XXX or 47,XXY n = 4; triploidy n = 4), and in samples from 348 matched controls. In the control group, SP1 increased significantly with fetal crown-rump length (r = 0.20, P < 0.0001) and there was no significant association with fetal nuchal translucency thickness (r = 0.03). Similarly, in the group with fetal chromosomal abnormalities, SP1 increased significantly with crown-rump length (r = 0.31, P < 0.01) and there was no significant association with nuchal translucency thickness (r = -0.08). In the groups with fetal trisomy 18 and trisomy 13, the median SP1 (0.76 MoM and 0.57 MoM, respectively) was significantly lower than in the controls (z = 2.64 and z = 3.27, respectively); in 21% and 25% of the cases, values were below the 5th centile. In the group with trisomy 21 and other chromosomal abnormalities the median SP1 (0.96 MoM and 0.93 MoM, respectively) was not significantly different from controls (z = 1.17 and z = 0.67, respectively). Measurement of SP1 concentration at 10-13 weeks' gestation is not likely to be useful in the prediction of fetal chromosomal abnormalities.

In hypoxemic intrauterine growth-retarded fetuses (IUGR) there is a reduction in the incidence of fetal movements and in fetal heart rate variation. A causal relationship with the impairment of fetal oxygenation has been suggested. In 16 IUGR fetuses and in 13 normally grown fetuses maternal hyperoxygenation was applied for 40 min to increase fetal PO2 levels. All IUGR fetuses had abnormal Doppler blood velocity waveforms of the umbilical artery suggesting an impaired uteroplacental exchange. The effect of hyperoxygenation on fetal breathing and body movements and on fetal heart rate was evaluated. In the IUGR fetuses there was a significant increase in fetal breathing and body movements and in heart rate variation during hyperoxygenation as compared to the preceding control period of 40 min. No significant changes in fetal breathing and body movements were found in the normally grown control fetuses. A surprising observation was the increase of the number of heart rate decelerations after discontinuation of the maternal hyperoxygenation. It is concluded that in IUGR fetuses the increase in fetal heart rate variation and the increase in the incidence of breathing and body movements during maternal hyperoxygenation substantiates the relationship between these variables and the oxygenation status of the fetus.

In 70 intrauterine growth-retarded (IUGR) fetuses with antepartum late heart rate decelerations recordings of velocity waveforms of the umbilical artery were made with Doppler ultrasound and calculated as pulsatility indexes (PI). In 29 of these fetuses longitudinal recordings were made. Abnormal PIs preceded the occurrence of late heart rate decelerations in 27 (93%) of the 29 fetuses. The median duration of the interval between the first abnormal PI and the first appearance of antenatal heart rate decelerations was 17 days (range 0-60 days). This wide range can mainly be attributed to the gestational age at which the first abnormal velocity wave-form was recorded; during early gestation the interval was much longer than later in pregnancy. Absent end-diastolic velocity (AEDV) was found in 17 of the 29 fetuses (59%) and preceded the occurrence of decelerations with a median interval of 12 days. In the total group, 4 of the 70 IUGR fetuses with antepartum decelerations had a normal velocity waveform of the umbilical artery. Fetuses with AEDV (n = 45) were more severely growth retarded and were delivered at an earlier gestational age than those with end-diastolic velocity (n = 25). Also perinatal mortality and morbidity were higher in the group with AEDV. Yet, when fetuses were matched for gestational age and birth weight no differences in perinatal outcome were found in the groups with and without end-diastolic velocity.