MATERNAL ACIDOSIS AND FETAL GROWTH RETARDATION

Abstract

Experience with infants born to mothers suffering from ketoacidosis has suggested that acidosis may be involved in fetal growth retardation (FGR). These studies were designed to determine the effect of acidosis on fetal substrate availability as reflected in altered uterine carbohydrate metabolism. Five pregnant ewes of 90-120 days gestation were chronically prepared by surgical implantation of bilateral electromagnetic uterine artery flow transducers and femoral and uterine vein catheters, and unilateral femoral and cystic artery catheters. Following a 4 day recovery period with optimum maternal nutrition, ammonium chloride solution was continuously infused to produce systemic maternal metabolic acidosis. Whole blood samples for glucose assay and acid-base studies were drawn at hourly intervals for 1-5 hrs in 5 ewes and hourly lactate assay in 1 ewe. Uterine glucose uptake and lactate production were calculated by the Fick equation. A total of 29 infusion studies were completed. The infusions produced no significant alterations in maternal glucose concentrations or uterine blood flow. Samples drawn after 4 hr. of acidosis demonstrated a significant decrease in maternal pH (p<.100), and uterine glucose uptake decreased by 55% (p<.05). Lactate production also decreased. We conclude that short term acidosis may decrease fetal substrate availability and that acidosis may play a significant role in the production of fetal growth retardation.