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Background. We hypothesized that ephedrine and phenylephrine are equal with respect to uterine and placental haemodynamics and fetal acid–base status after exposure to maternal hypoxaemia and hypotension in a chronic sheep model of increased placental vascular resistance (RUA). Methods. At 114–135 days gestation, chronically instrumented fetal sheep underwent placental embolization leading to increased RUA. Twenty-four hours after embolization, the ewes were anaesthetized and randomized to receive boluses of ephedrine (n=7) or phenylephrine (n=6) for epidural-induced hypotension after maternal hypoxaemia. Uterine (QUtA) and placental (QUA) volume blood flows and uterine vascular resistance (RUtA) and RUA were recorded. Uterine (PIUtA) and umbilical artery (PIUA) pulsatility indices were obtained by Doppler ultrasonography. Fetal arterial blood samples were analysed for acid–base values and lactate concentrations. Results. During hypotension, QUtA, fetal pH, BE, and Po2 decreased whereas RUtA, PIUtA, RUA, and fetal lactate concentration increased. With ephedrine, QUtA, RUtA, PIUtA, RUA, and fetal Po2 returned to baseline. Fetal pH, BE, and lactate concentration did not change from hypotensive values. With phenylephrine, QUtA remained lower (P=0.007) and RUtA (P=0.007), PIUtA (P=0.013), and RUA (P=0.050) higher than at baseline. Fetal Po2 returned to baseline and fetal pH and BE did not change from hypotensive values. However, fetal lactate concentration increased further (mean difference 1.49, 95% confidence interval 0.72–2.26 mmol litre−1; P=0.004). Conclusions. In a chronic sheep model of increased placental vascular resistance, compared with ephedrine administration, phenylephrine administration was associated with impaired uterine and placental haemodynamics and increased fetal lactate concentrations.

Background. Recent studies support the use of α-agonists during regional anaesthesia in uncomplicated term pregnancies. We hypothesized that ephedrine and phenylephrine, administered for maternal hypotension following fetal hypoxaemia, are equal in respect of fetal outcome. Methods. At 117–132 days gestation, chronically instrumented, anaesthetized and mechanically ventilated ewes were randomized to receive boluses of ephedrine (n=9) or phenylephrine (n=8) for maternal epidural-induced hypotension after a period of fetal hypoxaemia. Uterine (QUtA) and placental (QUA) volume blood flows were measured with perivascular transit-time ultrasonic flow probes, and uterine (RUtA) and placental (RUA) vascular resistances were computed from volume blood flows and maternal and fetal mean arterial pressures. Uterine (PIUtA) and umbilical artery (PIUA) pulsatility indices were obtained by Doppler ultrasonography. Results. Ephedrine increased QUtA and decreased RUtA and PIUtA from a hypotensive to baseline level and had no significant effect on umbilical circulation. With phenylephrine, QUtA remained lower (P=0.011) and RUtA higher (P=0.043) than at baseline, although PIUtA decreased to baseline level. PIUA increased from baseline with phenylephrine (P=0.007), whereas QUA decreased (P=0.050). Maternal volume expansion with hydroxyethyl starch decreased RUtA significantly irrespective of the vasopressor used. There were no significant differences in fetal blood gas values or lactate concentrations between the ephedrine and phenylephrine groups. Conclusions. Despite the more favourable effects on uterine and placental circulations of ephedrine over phenylephrine, no significant differences in fetal acid–base status or lactate concentrations were observed.