Effect of maternal oxygen inhalation on the fetus with growth retardation.

Decreased nutrient and oxygen transfer to the fetus accounts for fetal growth retardation in pregnancies complicated by severe uteroplacental insufficiency. A model of uteroplacental insufficiency was produced by ligation of the uterine artery of one horn in pregnant rats at 17 days of gestation. The pregnant rats were assigned to environmental chambers containing a gas mixture of either an increased fractional inspired oxygen concentration of 0.40 (O2) or room air from day 17 through 21 of gestation. Supplemental oxygen inhalation resulted in increased survival of the fetuses from the ligated horn [34 +/- 6% in intrauterine growth retardation (IUGR)-room air versus 57 +/- 8% in IUGR-O2] and an increase in fetal weight, expressed as a percentage of nonligated appropriate for gestational age control littermates (67 +/- 2% in IUGR-room air versus 74 +/- 2% in IUGR-O2). A role for hypoxia in the suppression of fatty acid synthesis in IUGR fetal tissues had been postulated; however, maternal oxygen inhalation did not result in any increase in fatty acid content or specific activity in liver, lung, or carcass of IUGR fetuses. These data indicate that supplemental maternal oxygen inhalation improves survival and growth of fetuses compromised by uteroplacental insufficiency, but it has no apparent effect on lipogenesis at term.