Maternal plasma progesterone levels in sheep may fall dramatically druing the last few days of gestation and following the administration of glucocorticoids to the foetus. To investigate the mechanism of the fall, metabolism of [3H] progesterone in vitro by ovin placental tissue was studied in five ewes before and after intra-foetal administration of dexamethasone in a dosage sufficient to induce parturition, and in one ewe after the spontaneous onset of labour at 143 days of gestation. Manual separation of maternal and foetal placental tissues showed that, in 11 out of 12 cases, the foetal and not the maternal placenta produced progesterone from pregnenolone in vitro. Total activities of cholesterol side-chain cleavage enzyme and 3beta-hydroxysteroid dehydrogenase in the foetal placenta were not influenced by intra-foetal dexamethasone. Befre administration of dexamethasone, homogenates of foetal placenta converted [3H] progesterone to 20alpha-hydroxy [3H]pregn-4-en-3-one in the presence of NADPH. Within 12 h of administration of dexamethasone, and after the natural onset of labour at 143 days, large amounts of 17alpha, 20alpha-dihydroxyI1pregn-4-en-3-one were formed form [3H]progesterone. Intra-foetal dexamethasone treatment also induced the formation of 17alpha, 20alpha-dihydroxy[3H]pregn-4-en-3-one by miced foetal placental tissue incubated with [3H]pregnenolone. This change in steroid metabolism did not occur in foetal placental tissue from a sham-operated animal receiving no dexamethasone. Assay of progesterone in foetal placentae showed that the increased fromation of 17alpha,20alpha-dihydroxypregn-4-en-3-one was unlikely to be caused by a change in the specific activity of added 3H-labelled precursor, although the production of 17alpha, 20alpha-dihydroxypregn-4-en-3-one in vitro increased at a time when both foetal placental and utero-ovarian venous levels of progesterone were decreasing in response to dexamethasone treatment. These observations indicate that intra-foetal dexamethasone treatment induces a placental 17alpha-hydroxylase enzyme, which is also present in foetal placental tissue after the spontaneous onset of labour at term.
Summary. The intrapartum cardiotocographs (CTGs) of 38 severely asphyxiated, term infants, born during a 17‐month period, and those of 120 healthy term infants acting as controls were independently reviewed by three investigators who were unaware of the clinical outcome. Interobserver agreement was good (Kappa statistic = 0.74, P<0.0001). The investigators found that cardiotocographic abnormalities were present in 33 of the asphyxiated infants (87%) and in 35 of the controls (29%) and predicted that the abnormalities were severe enough to lead to significant fetal metabolic acidosis at delivery in 23 asphyxiated infants (61%) and in 11 controls (9%). The differences between the two groups were highly significant (P<0.001). Using the traditional diagnostic criteria for fetal distress, the investigators found that fetal blood sampling was indicated in 58% of cases in the asphyxia group and in 20% of controls but was only performed in 16% of asphyxiated infants and in 8% of controls. Furthermore, the median response times of delivery suite staff for abnormal fetal heart rate patterns were similar whether the FHR changes, classified using Krcbs' CTG scoring system, were moderate or severe: 80 min and 90 min, respectively. These findings suggest that interpretation of the intrapartum CTG continues to pose major problems for practising obstetricians.
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