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OBJECTIVE: We attempted to determine changes occurring with time in fetal heart rate and its variation in fetuses with intrauterine growth retardation in whom late antepartum fetal heart rate decelerations eventually develop. STUDY DESIGN: Thirteen fetuses with intrauterine growth retardation were studied over a median period of 25 days. One-hour fetal heart rate records were made two to five times per week and were analyzed numerically. Fetal movements were recorded by the women. RESULTS: On average long-term fetal heart rate variation decreased gradually with time and fell below the norm (30 milliseconds) at about the same time decelerations appeared. Mean heart rate showed a slight but statistically significant increase after the occurrence of decelerations. There were large interfetal differences in all parameters studied. CONCLUSION: In fetuses with intrauterine growth retardation a decrease in long-term fetal heart rate variation is a rather late sign of impairment that coincides with the occurrence of late decelerations. In the surveillance of the fetus with intrauterine growth retardation it might be most appropriate to use each fetus as its own control. (Am J Obstet Gynecol 1992; 166: 22-7.)

Antenatal betamethasone administration to enhance fetal lung maturation is associated with transient reductions in fetal heart rate (FHR) variation, breathing, and body movements 2 d after the first dose (d 2). This study examines whether steroid administration affects the natural diurnal rhythms of fetal variables. Sixteen women at 27–32 wk of gestation received two doses of betamethasone 24 h apart. One-hour recordings of FHR, breathing, and body movements were made in the morning, afternoon, and evening of d 2, and again in the morning of d 3. Repeat recordings were obtained at 4–6 d later from 9/16 women. Maternal blood samples were obtained with each recording to determine ACTH and cortisol. No diurnal rhythm was present for FHR, FHR variation, breathing, and body movements on d 2. This resulted from suppression of the expected natural rise in body and breathing movements, and heart rate variation in the course of the day. Suppression of the diurnal rhythm of body movements depended on gestation (R−0.89; p< 0.01). All variables showed diurnal rhythms 4–6 d later. Maternal ACTH and cortisol diurnal rhythms were completely suppressed on d 2. Four to six days later, the normal diurnal pattern was resumed, although absolute levels of ACTH and cortisol were still suppressed. We conclude that maternal betamethasone administration transiently abolishes the fetal diurnal rhythms of heart rate and its variation, breathing, and body movements.

The short-term (0–48 h) effects of maternal betamethasone administration on computerized fetal heart rate (FHR) parameters were studied in 36 pregnancies at increased risk for preterm delivery. FHR was recorded for 90 min immediately before the start of betamethasone treatment and again at 6-h intervals during the next 48 h. Multiple linear regression models were used to assess the possible effects on FHR parameters of gestational age, time of day, clinical indication for treatment, and use of tocolytic drugs. Within 12 h after the start of treatment, significant increases occurred in FHR accelerations, and short- and long-term FHR variability (36%, 28%, and 22%, respectively), whereas basal FHR showed a 5% decrease. FHR variability was decreased by 10% at 42–48 h. The observed changes were more pronounced in older (29–33 wk of gestation) compared with younger fetuses (25–28 wk of gestation). Decelerations occurred only in 4 out of 11 compromised fetuses during betamethasone therapy. We conclude that there are significant changes in FHR parameters during the first 48 h after betamethasone administration. These changes are transient in normal fetuses. However, the compromised fetus may be adversely affected by betamethasone.

The efficacy of antenatal corticosteroid therapy in reducing the incidence of respiratory distress syndrome in twin pregnancy is controversial. The corticosteroid levels achieved with the current regimen might not be high enough to reach both siblings. In singleton fetuses, maternal betamethasone administration causes transient reductions in fetal heart rate (FHR), FHR variability, and body and breathing movements. We performed a prospective study to determine whether there are similar effects of betamethasone on FHR and behavior in preterm twin pregnancy and whether the effects occur similarly in both twin members. Eighteen women who were carrying twins received optimal corticosteroid treatment. Simultaneous recordings were made on twins before (day 0), during (days 1–2), and after (days 3–4) corticosteroid therapy using separate cardiotocography and ultrasound machines. Betamethasone administration was associated with significant transient decreases in basal FHR (day 1), FHR variability (days 2 and 3), and body and breathing movements (day 2). The overall changes in twins were similar to those previously found in singleton pregnancies. There was a high degree of association of response to betamethasone among individual members of twin pairs. The betamethasone-induced effects were unrelated to fetal sex, positioning, chorionicity, and discordance in size, but there was an effect of gestation on FHR. We conclude that the current regimen of antenatal corticosteroids used in preterm twin pregnancies results in observable physiologic and behavioral changes in twin pairs irrespective of their composition. This provides evidence that the achieved beta-methasone levels are high enough to reach the compartment of either twin member.

Objective : We examined whether psychological and endocrinological measures of stress during pregnancy predicted developmental outcome of human infants in a prospective design. Methods : Self-report data about daily hassles, pregnancy-specific anxiety and perceived stress, salivary cortisol levels and adrenocorticotropic hormone (ACTH) levels were collected in nulliparous women throughout pregnancy. Infant development was measured at 3 and 8 months by means of the Bayley Scales of Infant Development (BSID). Infant temperament was rated by means of observed behavior and maternal report. Results : High levels of pregnancy-specific anxiety in early pregnancy predicted both temperamental and developmental difficulties. High amounts of daily hassles in early pregnancy were associated with lower mental developmental scores. Perceived stress in early pregnancy was related to more difficult behavior and adaptational problems. Early morning values of cortisol in late pregnancy were negatively related to both mental and motor development, whereas higher ACTH levels were related to more adaptational problems. All results were adjusted for a large number of covariates. Conclusion : Increased maternal prenatal stress seems to be one of the determinants of temperamental and developmental variation of infants. The hypothalamic-pituitary-adrenal (HPA) axis may be involved in the harmful effects of prenatal maternal stress on infant development and temperament.

Determination of S-100 a and b and neuron-specific enolase (NSE) in (cord) blood and amniotic fluid has been used to assess neonatal neuronal damage after compromising conditions. However, these proteins are not only found in nervous tissue, and their expression in placenta and umbilical cord has never been investigated. In this study, S-100 (a and b) and NSE expression in human cord and placental tissue was studied by immunohistochemical analysis. Similar analysis was performed using two other brain-specific markers glial fibrillary acidic protein and growth-associated protein B-50 (also known as GAP-43 or neuromodulin). Tissue was derived after elective cesarean section in seven women of different gestational ages after uncomplicated or complicated pregnancy. S-100 a and b and NSE immunoreactivity was found in several cell types and structures in the umbilical cord as well as in the placenta of all seven cases. Glial fibrillary acidic protein and B-50 showed no immunoreactivity. These data are of importance for interpreting findings of studies in which S-100 or NSE levels in cord blood or amniotic fluid have been related to neuronal damage in the neonate. The increased levels found may just as well be caused by leakage from placenta or umbilical cord as be caused by brain damage. We conclude that S-100 a and b and NSE are not suitable markers for neonatal brain damage. Brain-restricted proteins such as glial fibrillary acidic protein and B-50 seem more promising.