Maternal, fetal and neonatal effects of beta-adrenergic stimulation in connection with cesarean section

To investigate the combined metabolic effects of beta-mimetic therapy and general anesthesia on maternal and fetal/neonatal metabolism, 14 patients were treated with isotonic saline, 11 with intravenous fenoterol (3 microgram/min) and 9 with intravenous isoxsuprine (150 microgram/min) for 30 minutes prior to cesarean section. The maternal heart rate and blood pressure as well as the maternal and fetal acid-base balance were followed. The neonatal glucose level was monitored for 36 hours after delivery. The heart rate and the diastolic and systolic blood pressure values increased during the operation in each group, without any marked differences between the groups. At delivery, the mean maternal BD (base-deficit) value was higher in the fenoterol patients than in the control patients, indicating a trend towards metabolic acidosis. The other values of acid-base balance in the maternal and umbilical arterial and venous blood did not reveal any differences between the groups. The neonatal glucose level at 2 hours after delivery was higher in the fenoterol group than in the control group. The other values recorded during 36 hours revealed no differences between the groups. Beta-mimetic treatment preceding general anesthesia in cesarean section does not have unfavorable effects on the mother, the fetus or the newborn. Such therapy thus does not seem contraindicated when uterine contractions should be rapidly suppressed in cases of fetal distress before operation.     

Maternal and fetal prolactin in pregnancy-induced hypertension

Summary In plasma from 35 women with pregnancy-induced hypertension (PIH) and 35 normal pregnant women both at 39 weeks of gestation, plasma prolactin levels were measured at 8.30 a.m. (PRL1) and 9.30 a.m. (PRL2) under basal conditions. At delivery umbilical cord blood samples were taken for measurement of fetal prolactin (PRLF). PRL1 and PRL2 were higher in women with PIH, but no significant relations were found betwen PRL1/PRL2 and blood pressure. PRLF did not differ when infants of mothers with PIH and infants of normal pregnant women were compared, but PRLF had a significant direct independent relation with PRL2. The latter relation may be due to the increase in placental oestrogens during pregnancy, which stimulate both the maternal and fetal hypophyses and their prolactin secretion. PRLF did not show any relation with neonatal morbidity, but PRL1 showed a significant direct relation with the Apgar score at 5 min.     

Twin pregnancy as a model for studies in fetal cortisol concentrations in labour: relation to prostaglandins, prolactin and ACTH

Cortisol and prostaglandins were measured in umbilical cord blood obtained from 50 twin pregnancies at caesarean section performed either before or during labour. Umbilical artery cortisol concentrations did not differ between twin I and II before labour or in the latent stage. During active labour cortisol levels were significantly higher in twin I than in twin II. Maternal cortisol levels did not correlate with cord blood cortisol levels in either twin before active labour, nor did the rise in maternal cortisol correlate with the cortisol level in twin I; maternal cortisol levels did, however, correlate with cortisol levels in twin II during active labour. Prostaglandins E(PGE), F 2 alpha (PGF 2 alpha), 13,14-dihydro-15-keto F 2 alpha (PGFM) and ACTH were measured in cord vein blood. PGE values did not differ between twin I and II before active labour. During active labour PGE levels were significantly greater in twin I and correlated with raised cortisol levels. No differences were seen at any stage in PGE and PGFM levels between twins I and II although PGFM levels increased in both twins during active labour. ACTH and prolactin levels did not increase during labour and were similar in twins I and II. The rise in fetal cortisol during active labour is primarily of fetal origin and PGE may be involved in stimulating cortisol production in the fetus.     

Twin pregnancy as a model for studies in fetal cortisol concentrations in labour: relation to prostaglandins, prolactin and ACTH

Summary. Cortisol and prostaglandins were measured in umbilical cord blood obtained from 50 twin pregnancies at caesarean section performed either before or during labour. Umbilical artery cortisol concentrations did not differ between twin I and II before labour or in the latent stage. During active labour cortisol levels were significantly higher in twin I than in twin II. Maternal cortisol levels did not correlate with cord blood cortisol levels in either twin before active labour, nor did the rise in maternal cortisol correlate with the cortisol level in twin I; maternal cortisol levels did, however, correlate with cortisol levels in twin II during active labour. Prostaglandins E(PGE), F_2α(PGF_2α), 13,14-dihydro-15-keto F_2αPGFM) and ACTH were measured in cord vein blood. PGE values did not differ between twin I and II before active labour. During active labour PGE levels were significantly greater in twin I and correlated with raised cortisol levels. No differences were seen at any stage in PGE and PGFM levels between twins I and II although PGFM levels increased in both twins during active labour. ACTH and prolactin levels did not increase during labour and were similar in twins I and II. The rise in fetal cortisol during active labour is primarily of fetal origin and PGE may be involved in stimulating cortisol production in the fetus.     

Maternal serum cortisol and prolactin variations during labor.

Maternal serum cortisol (F) and prolactin (PRL) levels were measured during labor in 20 uncomplicated pregnancies. Four pregnant women were admitted with ruptured membranes (RM group) and 16 were admitted with intact membranes (IM group), ten with spontaneous onset of labor (SL group) and 10 with induced labor (IL group), five with a prolonged for duration labor (PL group) and 15 with a normal for duration labor (NL group). Before the inset of labor F levels were statistically higher (p less than 0.05) in the RM group (x = 975 ng/ml), than in the IM group (x = 664 ng/ml), and also in the SL group (x = 783 ng/ml), than in the IL group (x = 679 ng/ml). During labor, in all twenty pregnant women a marked rise of F (from x = 726 ng/ml before the onset of labor, to x = 911 ng/ml) and a marked fall of PRL (from x = 161 ng/ml to x = 122 ng/ml) were observed (p less than 0.05). In the PL group the F elevation and the PRL drop were more pronounced (p less than 0.001). After placental separation, PRL levels increased slightly while F values remained unchanged. These changes in hormone levels before and during labor could be attributed to the emotional and physical stress of labor.     

Amniotic fluid prolactin and fetal lung maturation

Concentrations of prolactin in amniotic fluid, fetal plasma, and maternal plasma were determined in 34 rhesus monkeys delivered by hysterotomy under general anesthesia at gestational ages of 110 to 160 days (term, 165 days). Included were 15 cases (gestational ages 110 to 143 days) in which the mothers received 2 mg of betamethasone intramuscularly daily for 3 days prior to delivery. Fetal lung maximum volumes were determined in addition to the following indices of fetal lung surfactant: lung alveolar stability, lung phosphatidylcholine concentrations, lung extract surface tensions, and amniotic fluid lecithin to sphingomyelin ratios. Amniotic fluid prolactin was found to correlate significantly with lung alveolar stability (r = 0.51; p less than 0.01), lung phosphatidylcholine (r = 0.51; p less than 0.01), lung extract surface tension (r = -0.39, p less than 0.05) and amniotic fluid lecithin/sphingomyelin ratio (r = 0.50; p less than 0.01). These correlations remained statistically significant even when the effects of gestational age were taken into account. These findings suggest that amniotic fluid may modulate fetal production of surfactant via its prolactin content.     

Maternal and fetal plasma cortisol levels at parturition.

Fetal adrenal function during pregnancy has a probable role in parturition. Ninety-five mothers and fetuses were evaluated to ascertain maternal or fetal plasma cortisol interrelationships under various clinical situations. When mode of delivery was evaluated, maternal cortisol levels showed no differences. However, the fetuses from vaginal delivery (mean, 43.7 mug/100 ml) had higher levels than those from cesarean section (mean, 34.7 mug/100 ml). Induction of labor showed a rise in maternal cortisol from preinduction levels (mean, 40.2 mug/100 ml) to delivery (mean, 49.6 mug/100 ml), probably reflecting the maternal stress of labor. The fetal cortisol level after induced labor (mean, 35.2 mug/ml) supporting the adrenal contribution to the initiation of labor. Gestational age of the fetus was significant in the fetal cortisol levels: 36 weeks or less (mean, 34.1 mug/100 ml); 37 weeks or more (mean, 44.5 mug/100 ml). This again supports the development of adrenal maturity. Fetal weight, postdatism, acute and chronic fetal distress, hypertensive disease in pregnancy, and race were evaluated without revealing any significant intergroup differences. Two anencephalic pregnancies were also studied.     

Decidual, amniotic fluid, maternal and fetal prolactin in normal and abnormal pregnancies

In the present studies, the content and the in vitro production of prolactin by decidua as well as the concentrations of prolactin in amniotic fluid, maternal and fetal serum in normal term pregnancies, induced abortions at various gestational ages, and in pregnancies complicated by diabetes mellitus, preeclampsia, chronic hypertension, and polyhydramnios were measured. Maternal and fetal prolactin levels varied considerably throughout gestation, but at term did not differ significantly between normal and abnormal pregnancies. Prolactin levels in amniotic fluid as well as decidual prolactin content and production were significantly lower only in pregnancies complicated by either hypertension or polyhydramnios. In both normal and abnormal pregnancies, decidual prolactin production correlated strongly with amniotic fluid concentrations. The present data suggest that 1) maternal and fetal prolactin levels do not differ significantly between normal and abnormal pregnancies, 2) the decidua is the principal source of amniotic fluid prolactin, and 3) the significantly lower levels of prolactin in amniotic fluid of pregnancies complicated by hypertension or polyhydramnios are probably due to adverse effects of these conditions on the synthesis and release of prolactin by decidua.     

Maternal plasma and amniotic fluid prolactin levels in normal and hypertensive pregnancy

Prolactin levels in the plasma and amniotic fluid of 121 normal pregnant women, 78 women with pre-eclampsia and 30 women with essential hypertension complicating pregnancy were determined by radioimmunoassay. Mean prolactin levels in plasma, but not in amniotic fluid, were significantly lower than controls in the group with pre-eclampsia (P less than 0.01) and in the group with essential hypertension (P less than 0.05). These findings suggest altered production and/or clearance of prolactin from the maternal compartment in these patients and may explain their increased response to pressor agents.     

Amniotic fluid cytokine profile in association with fetal hyperechogenic bowel

OBJECTIVES: Fetal hyperechogenic bowel (FEB) is associated with infection, chromosomal abnormalities and poor fetal outcome. FEB may result from an intrauterine fetal bowel cytokine-mediated inflammatory response. Since alterations in the levels of the cytokines interleukin (IL)-6, IL-8, IL-10, tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma are associated with pregnancy complications and necrotizing enterocolitis, this study aimed: (i) to determine their involvement in the pathophysiology of FEB and (ii) to identify their role as amniotic fluid markers of this condition. STUDY DESIGN: In this prospective case-control study, amniotic fluid was collected by transabdominal amniocentesis from pregnant women with fetuses presenting (n=10)--or not (n=30)--with FEB during routine 18-20 week ultrasound scans. Cell-free amniotic fluid samples were analysed for cytokine concentrations by fluid-phase multiplex immunoassay. Data were compared by Mann-Whitney U-tests and Pearson correlations. RESULTS: Amniotic fluid IL-8 levels were significantly higher in the FEB group. There was a positive correlation between IL-6 and each of IL-8 and INF-gamma, as well as between IL-8 and IL-10, and TNF-alpha and INF-gamma. CONCLUSIONS: FEB likely ensues from a fetal inflammatory process involving IL-8 and, possibly, IL-6 and IL-10. This indicates the potential of immunomodulatory therapy in the management of FEB.     

Maternal serum activin A levels in association with intrauterine fetal growth restriction

Objective To assess maternal serum activin A as a potential marker of fetal growth restriction.
Design A cohort study.
Setting A maternal–fetal medicine unit, university teaching hospital.
Population Fifty-seven women with a small fetus (less than 10th centile for gestation) referred for assessment of fetal size by ultrasound biometry.
Methods At the time of presentation for fetal biometry, maternal blood was collected for activin A measurement. The case records of each woman were independently reviewed after delivery and the pregnancy grouped into one of three groups: constitutionally small fetus, intrauterine growth restricted (IUGR) fetus or IUGR fetus and maternal pre-eclampsia (IUGR–pre-eclampsia). Activin A levels in the three groups were compared.
Main outcome measures Maternal serum activin A levels.
Results Sixteen of the 57 pregnancies were classified as constitutionally small, 17 as IUGR and 24 as IUGR–pre-eclampsia. Expressed as multiples of a normal median (MoMs), the median (95% CI) activin A level in the constitutionally small pregnancies was 1.12 (0.72–1.39) MoMs significantly lower than the level in both the IUGR pregnancies, 3.00 (1.84–4.11) MoMs, and the IUGR–pre-eclampsia pregnancies, 7.96 (5.73–10.62) MoMs (   P = 0.002 and 0.0001 for IUGR vs constitutionally small and IUGR–pre-eclampsia vs constitutionally small, respectively  ).
Conclusions Maternal serum activin A may be useful in the assessment of the small for gestational age fetus.     

Maternal and fetal serum prolactin levels in cases of premature rupture of membranes

Serum prolactin levels were measured in maternal and fetal sera immediately post delivery in 20 cases of premature rupture of the membranes and in 20 controls. Fetal serum prolactin levels were 781 +/- 265 ng/ml in cases of PRM and 737 +/- 314 ng/ml in controls. Maternal serum prolactin levels were 504 +/- 264 ng/ml in cases of PRM and 731 +/- 361 ng/ml in controls. This difference is statistically significant (t = 1.81, p less than 0.05). A probable role of prolactin in maintaining fetal membrane integrity and the probable effect of the difference in maternal serum prolactin concentration in the two groups on the membranes' viscoelastic properties is discussed.     

Maternal plasma and amniotic fluid levels of estradiol, estrone, progesterone, and prolactin in early pregnancy

During the 16th to 20th weeks of gestation, maternal plasma (mean) level of estradiol is 5.2 ng/mL; estrone, 3.0 ng/mL; estriol, 2.1 ng/mL; progesterone, 4235 ng/dL; and prolactin, 74 ng/mL. Amniotic fluid levels are: estradiol, 446.8 pg/mL; estrone, 234.1 pg/mL; progesterone, 5200 ng/dL; and prolactin, 2633.5 ng/mL. Maternal prolactin concentrations correlate with plasma estradiol. Amniotic fluid prolactin levels correlate significantly with maternal plasma concentrations of estradiol and estrone. The mechanisms for the possible relationship between maternal estradiol and pituitary and decidual tissue production of prolactin are discussed.     

Maternal and fetal factors related to abnormal amniotic fluid.

OBJECTIVE: The objective of this study was to identify maternal and infant characteristics related to alteration of amniotic fluid volume at birth. STUDY DESIGN: A series of 27,145 consecutive malformed newborn infants from the Spanish Collaborative Study of Congenital Malformations (ECEMC) was analyzed. From this total, 3.01% were found to have oligohydramnios and 3.69% were found to have polyhydramnios. RESULTS: As expected, renal/urinary tract and lung defects were associated with oligohydramnios, whereas esophageal and intestinal atresias, neural tube defects, and other central nervous system malformations were associated with polyhydramnios. In addition, other defects such as cardiovascular anomalies, hydrocephaly, and microcephaly were also related to abnormalities of amniotic fluid volume. After excluding the defects whose association to oligo- or polyhydramnios is well recognized, we compared the frequency of different variables among them and with infants with a normal volume of amniotic fluid. In comparison with infants with normal amniotic fluid volume, the groups with oligo- and polyhydramnios had lower birth weight, shorter gestational age and umbilical cord, higher parental ages, and a greater frequency of spontaneous abortions. The differences were more marked for weight in newborn infants with oligohydramnios, and for gestational age, umbilical cord length, number of previous pregnancies, and spontaneous abortions in polyhydramnios cases. Placental weight was lower in oligohydramnios cases than in infants with normal amniotic fluid, and higher in polyhydramnios cases. Parental consanguinity and twinning were more frequent in polyhydramnios. Maternal morbidity was higher in both groups with abnormal amniotic fluid volume, especially for acute diseases such as hypertension, diabetes mellitus, and gestational diabetes. Chromosomal aberrations were more frequent in the oligo- and polyhydramnios groups than in cases with a normal volume of amniotic fluid, which supports the suggestion of performing prenatal cytogenetic analysis in any pregnancy complicated by an abnormal volume of amniotic fluid. CONCLUSION: The fact that all of these results are similar in the control group of healthy infants suggests that at least some of the variables associated with abnormal amniotic volume could be considered as causal factors altering the production of fluid.