SummaryThirty nulliparous patients with a Bishop score of 4 or less had labour induced with prostaglandin E, in triacetin gel, initial dose 2 mg, with Further doses of 1 or 2 mg at 6 and 12 h if required. Seventeen of 27 patients (63 per cent) were in established labour and required no further stimulation by 18 h. The mean induction to delivery interval was 13 h. Eight more patients proceeded to vaginal delivery with the aid of oxytocin stimulation, with a mean induction to delivery interval of 38·5 h. Thus 93 per cent achieved vaginal delivery. Patients not responding to a total dose of 4 mg are unlikely to have successful induction with further doses of prostaglandin E, gel.

(1994). Sturge-Weber syndrome associated with transient hydrops fetalis. Journal of Obstetrics and Gynaecology: Vol. 14, No. 3, pp. 162-163.

Fetal macrosomia (FM) is a well-recognized complication of diabetic pregnancy but it is not known whether placental transport mechanisms are altered. We therefore studied the activity of the system A amino acid transporter, the system L amino acid transporter, and the Na+/H+ exchanger in microvillous membrane vesicles from placentas of macrosomic babies born to diabetic women (FM group), from placentas of appropriately grown babies born to diabetic women (appropriate for gestational age group) and from placentas of appropriately grown babies of normal women (control group). Sodium-dependent uptake of [14C]-methylaminoisobutyric acid at 30 s (initial rate, a measure of system A activity) was 49% lower into FM vesicles than into control vesicles (P < 0.02); this effect was due to a decrease in Vmax of the transporter with no change in Km. There was no significant difference in system A activity between the appropriate for gestational age group and control or FM group. There was also no difference between system L transporter or Na+/H+ exchanger activity between the three groups. We conclude that the number of system A transporters per milligram of membrane protein in the placental microvillous membrane is selectively reduced in diabetic pregnancies associated with FM.

Placentas of anesthetized rats were perfused in situ on the fetal side to study mechanisms of Mg2+ transport. The perfusate was a Mg(2+)-free Krebs-Ringer, and the unidirectional transfer of Mg2+ from maternal plasma to this Ringer was compared with that of 45Ca and 51Cr-EDTA, the latter being employed as a paracellular diffusional marker. Placental perfusion with amiloride (0.5 mM) or ouabain (1 mM) both rapidly (4 min) reduced maternal-fetal clearance (Kmf) for Mg2+ but had no effect on Kmf for 45Ca. In contrast, perfusion of the carbonic anhydrase inhibitor acetazolamide (1 mM) did not affect Kmf for Mg2+ or 45Ca. Placental perfusion with a Na+-free Ringer reduced Kmf for both Mg2+ and 45Ca, although the latter response was delayed. Kmf for 51Cr-EDTA was increased by amiloride and was unaffected by perfusion of ouabain, acetazolamide, or Na+-free Ringer, indicating that the effects of these treatments on Kmf of Mg2+ do not reflect nonspecific effects on placental permeability. These data suggest that maternal-fetal transfer of Mg2+ across the perfused rat placenta is Na+ dependent.

Two human parathyroid hormone-related protein (hPTHrP) fragments were tested for effects on maternofetal transfer of 45Ca and Mg across the in-situ perfused rat placenta at 21 days of gestation (term = 23 days). The fetal placental circulation was perfused with a Mg-free Krebs-Ringer solution and the unidirectional maternofetal clearance (Kmf) of 45Ca and Mg compared with that of 51Cr-EDTA, the latter being employed as a paracellular diffusional marker. Placental perfusion with hPTHrP(1-34) (100 ng/ml) or hPTHrP(75-86)amide (50 ng/ml) did not significantly alter the Kmf of 45Ca or that of Mg. In separate rats, however, hPTHrP(1-34) but not hPTHrP(75-86)amide stimulated marked placental cyclic AMP (cAMP) release, the peak response of 63 +/- 7 pmol/min occurring 10 min after the beginning of the peptide perfusion. A lower dose of hPTHrP(1-34) (4 ng/ml) produced a similar peak release of cAMP, as did [Nle8,21, Tyr34]-rPTH(1-34)amide (4 ng/ml) and the adenylate cyclase agonist forskolin (17 mumol/l). Forskolin also rapidly increased the Kmf of 45Ca but not that of Mg or 51Cr-EDTA. The present study indicates that hPTHrP does not acutely affect maternofetal transfer of Ca or Mg across the perfused rat placenta. The data also question the role played by cAMP in the stimulatory actions of forskolin on placental Ca transport.

ABSTRACT: Mechanisms of maternofetal Mg transfer have been investigated across the in situ perfused rat placenta at 21 d gestation (term=23 d). The fetal placental circulation was perfused with Mg-free Krebs-Ringer solution and clearance of Mg from maternal plasma across the placenta [unidirectional maternofetal clearance (Kmf) Mg] compared with that for 45Ca and 51Cr-EDTA, the latter being used as a diffusional marker. Because diffusion coefficients determined for these solutes were similar (6.8-7.6 X 10~6 cm2-sec−1), greater Kmf values determined for Mg and 45Ca (mean ± SD: 26.7 ± 9.2 and 93.1 ± 29.8 nLmin−1 -g−1 placenta, respectively) compared to 51Cr-EDTA (3.2: 0.9 fiLmin '-g ') suggest that maternofetal transfer of these cations occurs by mechanisms in addition to diffusion. Kmf Mg was also greater than Kmf 5ICr-EDTA when measured across the dually perfused rat placenta, in which the maternal uterine artery was additionally perfused with Mg-containing (0.5 mmol-L−1) Krebs-Ringer solution. Decreasing the Mg concentration in the maternal perfusate by 90% reduced Mg appearance in the fetal perfusate by 87% within 8 min; this suggests that Kmf Mg across the in situ perfused placenta largely reflects Mg transfer from maternal plasma and not simply elution of a placental Mg pool. Addition of KCN (1 mmol-L−1) to the fetal perfusate or lowering perfusate temperature from 37 to 26°C significantly reduced Kmf Mg and Kmf 45Ca across the in situ perfused placenta. In contrast, Kmf 51Cr-EDTA was increased by KCN and unaffected by temperature. Both total and ultrafiltrable Mg concentrations were higher in fetal compared with maternal plasma, indicating that maternofetal Mg transfer occurs against a chemical gradient. These data collectively suggest that maternofetal transfer of Mg, as well as that of Ca, is dependent on placental metabolism. (Pediatr Res 27: 622-625, 1990