1. Cerebral blood flow and cerebral metabolism were measured in conscious, normally grown neonatal piglets and in littermates which had undergone intrauterine growth retardation. 2. Cerebral blood flow was measured by the Kety-Schmidt technique using [ 125 I]iodoantipyrine as the tracer. The tissue: blood partition coefficient of this tracer was measured in separate groups of growth retarded and normal animals. Cerebral utilization rates of glucose and oxygen were calculated from the arteriovenous concentration differences on the Fick principle. 3. The mean body weight of the growth retarded animals was about half that of their normally grown littermates, and liver weight was reduced in proportion. Brain weight was slightly but significantly lower in the growth retarded animals. 4. Cerebral blood flow was lower in the growth retarded piglets but the rates of cerebral utilization of oxygen and glucose were not significantly different in the two groups. The fractional extraction of arterial oxygen by the brain was significantly higher in the growth retarded animals. 5. The partition coefficient of ipdoantipyrine was significantly lower in the growth retarded animals, being about 75% of the normal value. It is clear that had the partition coefficients been assumed to have been the same in both groups the calculated cerebral blood flows would have been identical. 6. It is concluded that growth retarded neonatal piglets have relatively normal sized brains, with a rate of glucose and oxygen consumption that is not significantly different from normal, despite a reduction in cerebral blood flow of about 35%. Consequently the fractional extraction rate of arterial oxygen by the brain is increased from 50% to 70%.
1. Because studies of the metabolic problems of the human intra-uterine growth-retarded neonate are limited by ethical considerations we have used the intra-uterine growth-retarded piglet as an animal model. Total body-glucose kinetics were measured in 16 intra-uterine growth-retarded and 11 normal piglets from the same litters with [ 3 H]glucose as a tracer. 2. The intra-uterine growth-retarded animals had marginally smaller brains than their normal littermates, but substantially smaller livers. Liver weight was reduced in proportion to body weight. 3. Total body-glucose turnover rate was significantly lower ( P < 0.001) in the intra-uterine growth-retarded animals in comparison with their normal littermates, but was appropriate for their smaller body and liver weights. Brain weight was only slightly reduced in the intra-uterine growth-retarded group so that glucose turnover adjusted to a common brain weight was significantly lower ( P < 0.001) in these animals. 4. Total body-glucose pool size was lower in the intra-uterine growth-retarded animals ( P < 0.01), but was appropriate for their body and liver weights. It was significantly reduced in relation to brain weight ( P < 0.001). 5. Resting plasma glucose concentration was lower in the intra-uterine growth-retarded animals ( P < 0.001). There was no relationship between concentration and turnover in either group. 6. It is suggested that the observed differences in total body-glucose turnover may be associated with profound differences in cerebral metabolism in the intra-uterine growth-retarded animals.