Fetal Intravenous Nutritional Supplementation Ameliorates the Development of Embolization-Induced Growth Retardation in Sheep

Abstract
Since decreased transfer of nutrients into the fetus has been documented in many forms of intrauterine growth retardation, we evaluated whether increasing fetal nutrient availability would prevent the development of experimental growth retardation in fetal lambs. Fetuses were separated into three groups: E, animals growth retarded by repetitive uteroplacental embolization (n = 8); ES, animals treated as in E and given fetal femoral venous infusions of 5% glucose and 6.8% amino acids (n = 7); and C, controls (n = 8). The duration and density of embolization were the same in E and ES; initial physical and metabolic characteristics and gestation at delivery were similar in all groups. E birth weight was reduced 26% compared to C (2888 .+-. 373 SEM g versus 3880 .+-. 277 g, p < 0.05); fetal/maternal weight ratio was decreased 35% (p < 0.005) and ponderal index decreased 22% (p < 0.005). Asymmetric growth retardation was indicated in E by an increased brain/body weight ratio (p < 0.05). ES fetuses, in contrast, showed no differences from C in birth weight (3601 .+-. 190 g) or body proportions. ES were larger than E, with a greater fetal/maternal weight ration and ponderal index (p < 0.05 for both). In E and ES, size at birth showed a positive relation to the amount of supplements received. The average daily supplementation rate correlated with the fetal/maternal weight ratio and with the ponderal index (for both r = 0.62, p < 0.02). Within the ES group alone there was a marked correlation between the average daily supplementation rate and birth weight (r = 0.97, p < 0.001). Placental weight was reduced 36% in E versus C. but was maintained in ES (p < 0.02 E versus ES, p < 0.05 E versus C). In E and ES, placental size correlated with the volume of supplements received by the mid-third trimester (r = 0.84, p < 0.001). Along with the reduction in placental size, umbilical blood flow was decreased 27% in E versus ES (p < 0.05). Nutrients availability appeared to be a major determinant of the development of fetal and placental growth retardation in this study. However, the specific nutritional or metabolic factors leading to improved growth could not be identified.