The effects of partial amniotic carbon dioxide insufflation in an ovine model

We aim to assess the effect of partial amniotic carbon dioxide insufflation (PACI) at increasing pressures on fetal acid-base, fetal-placental perfusion, and fetal membrane morphology in an ovine model.

Pregnant ewes and fetuses were instrumented under isoflurane anesthesia at 105 days gestation (term 145 days) to monitor utero-placental blood flow, fetal and maternal blood pressure, heart rate, and blood gas status. One group (n = 6) was exposed to PACI (unheated dry CO₂ ), involving 10 mm Hg stepwise increases in insufflation pressure (5 to 25 mm Hg), for 80 minutes followed by 20 minutes of desufflation. Un-insufflated controls (n = 5) were monitored for 100 minutes. At postmortem, fetal membranes were collected for histological analysis.

PACI at 25 mm Hg caused severe fetal hypercapnia (PaCO₂  = 143 ± 5 vs 54 ± 5 mm Hg, P < 0.001), acidosis (pH = 6.85 ± 0.02 vs 7.25 ± 0.02, P < 0.001), hypoxia (SaO₂  = 31 ± 4% vs 57 ± 4%, P = 0.01), and reduced uterine artery flow (50 ± 15 vs 196 ± 13 mL/min/kg, P = 0.005) compared with controls. These effects were greater at higher PACI pressures. PACI resulted in leukocyte infiltration in the amnion (1.77 × 10^-5  ± 0.61 × 10^-5 vs 0.38 × 10^-5  ± 0.19 × 10^-5  cells/μm² , P = 0.04) and chorionic membranes (2.94 × 10^-5  ± 0.67 × 10^-5 vs 0.84 × 10^-5  ± 0.42 × 10^-5  cells/μm² , P = 0.01).

Higher PACI pressures results in larger disturbances in fetal acid-base, uterine blood flow, and fetal membrane inflammation in sheep. Differences between human and sheep utero-placental structure should be considered.