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The energy-rich substrates available to the fasting stressed baboon neonate and infant are quantitatively similar to the metabolic fuels presented to the stressed low birth weight human newborn. Within a few hours after birth, fasting arterial plasma glucose levels in the baboon neonate approximate those of 4–6-week-old baboon infants after a 20-hr fast. Lactate levels are high and comparable for both age groups. In contrast, β-hydroxyburyrate is quite low in the immediate neonatal period, but rises to significantly higher levels (P< 0.001) after a fast at 4–6 weeks. In addition, glycerol levels are higher (P< 0.02) in the fasted older infant compared with the fasting neonate.

Estimates of splanchnic energy substrate exchange in the primate infant have been obtained using a baboon model. The splanchnic bed of the fasting baboon newborn released glucose at an estimated rate of 14.5 ± 5.0 µmol/min·kg body weight. Splanchnic glucose release in the fasting 5-7-wk old baboon infant proceeded similarly at an estimated rate of 15.5 ± 4.5 µmol/min·kg body weight. The principal precursors taken up by the splanchnic bed were lactate, glycerol, and alanine. Uptake of alanine correlated in a linear fashion with glucose release. Lactate was the most important precursor in both age groups. Glucose recycling through lactate is an active mechanism in the primate fetus as well as in the young of other species.

Extract: Measurement of intrarenal distribution of renal blood flow by injection of radionuclides in 3—5-day-old infant monkeys showed a preponderance of outer cortical over inner cortical flow with flow rates of 4.23 and 2.54 ml/min/g, respectively. Intermittent positive pressure ventilation (IPPV) causes a reversal of this flow pattern. The theoretical difference in nephron function in these two areas suggests that this reversal in intrarenal flow induced by IPPV may have important clinical implications.Speculation: Extrarenal stimuli such as IPPV causes a redistribution of intrarenal blood flow in infant primates. Any stimuli that results in increased production of epinephrine or similar compounds may be responsible for this redistribution by a local effect on outer cortical blood vessels. Our data further suggest that antidiuretic hormone may influence intrarenal blood flow in addition to altering tubular membrane permeability.

The age-related changes in fasting arterial levels of energy substrates and insulin were studied at birth and/or 6 wk in eleven baboon infants. In addition, the renal contribution to glucose release in the primate infant was estimated. Arterial blood glucose levels were similar in six fasted newborns and in nine fasted 6-wk-old infants. Arterial blood lactate, alanine, pyruvate, glutamate, and glutamine levels were significantly higher (P< 0.01) in the new born animals, and β-hydroxybutyrate was significantly higher in the older animals (P< 0.001). Arterial plasma insulin levels were low in both groups. Levels of blood glucose in the inferior vena cava below the renal vein were significantly lower than levels in the aorta (P< 0.01). In contrast, levels of blood glucose in the inferior vena cava above the renal vein were significantly higher than in the aorta (P< 0.05). Computed renal vein glucose levels were higher than those in the aorta (P< 0.01). In the newborn infants, there was significant renal uptake of lactate, pyruvate, glycerol, and glutamine (P< 0.01), and release of β-hydroxybutyrate (P< 0.05). In the older animals, there was renal uptake of alanine, lactate, pyruvate, and glycerol (P0.01). Mean cardiac output per kg body weight did not differ significantly in the newborn and 6-wk-old infants.

We examined the effects of maternal sodium ß-hydroxybutyrate (NaBOHB) on the primate fetus to investigate the impact of ketosis not associated with acidosis on fetal metabolism. After a loading dose (600 mg/ kg), NaBOHB was infused for 70 min (300 mg/kg hr) into the maternal femoral vein of eight pregnant baboons, and placental transfer and fetal and maternal metabolic changes were observed during an acute experimental protocol. Maternal arterial levels rose from 0.70 ± 0.21 to 5.42 ± 0.93 mM (p<0.001), and fetal arterial levels from 0.34 ± 0.09 to 2.76 ± 0.64 mM (p<0.01). A maternalfetal gradient of approximately 21 was observed in both baseline and steady-state infusion conditions and is similar to the human maternal-fetal ketone gradient. This is in contrast to the sheep where significantly higher gradients have been described. The elevated lactate, from 1.90 ± 0.34 to 2.88 ± 0.54 mM (p<0.05) and somewhat decreased pO2values in the fetus from 54.8 ± 8.9 to 45.0 ± 3.8 mm Hg (p>0.05<0.1), without change in oxygen consumption (2.00 ± 0.28 versus 1.73 ± 0.15 mM/min) are features common to conditions of increased levels of fetal energy substrate. NaBOHB does not appear to contribute to oxidative energy metabolism of the whole fetus but may contribute to lipid stores. The significance of higher levels of BOHB in the primate fetus compared to the sheep fetus remains to be elucidated

Recent studies have shown that the fetal kidney is limited in its ability to acidify the urine and to secrete hydrogen ions when compared to the adult kidney. To further study H+secretion and the ability of the fetal kidney to establish a pH gradient between blood and urine, Na2SO4was infused into the intact fetus.Studies were done on 7 near-term pregnant sheep and their fetal lambs. The ewes were injected with DOCA and the fetuses were given cortisone acetate. This served to enhance renal tubular reabsorption of Na+. Caesarean sections were performed and 75cc of 8% Na2SO4was infused into each fetus. Blood and urine samples were collected from the ewe and fetus. There were no significant changes in fetal or maternal blood pressure, pulse, temperature or pCO2.The mean initial urine and blood pH in the fetus was 7.075 and 7.352 respectively. The mean minimum urine pH in the fetus after Na2SO4was 5.2 with a range of 4.7–5.7. The mean minimum blood pH in the fetus after Na2SO4was 7.362. The mean urine pH in the ewe before and after Na2SO4was 5.824 and 5.920 respectively. This is consistent with little or no transfer of SO4= across the placenta. The mean maximum TA and NH4excretion in the fetus was 4.35 and 8.21 µEq/min/kg respectively. There was no correlation between fetal weight and response time before production of an acid urine.These studies indicate that in the intact fetal lamb, a stimulus (DOCA) to the fetal kidney to reabsorb Na+without equivalent amount of anion results in intense acidification of the urine. The fetal kidney is thus able to establish a pH gradient with no evidence of intrinsic limitation of hydrogen ion secretion.