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Urea production may be impaired in intrauterine growth restriction (IUGR), increasing the risk of toxic hyperammonaemia after birth. Arginine supplementation stimulates urea production, but its effects in IUGR are unknown. We aimed to determine the effects of IUGR and arginine supplementation on urea production and arginine metabolism in the ovine foetus. Pregnant ewes and their foetuses were catheterised at 110 days of gestation and randomly assigned to control or IUGR groups. IUGR was induced by placental embolisation. At days 120 and 126 of gestation, foetal urea production was determined from [14C]-urea kinetics and arginine metabolism was determined from the appearance of radioactive metabolites from [3H]-arginine, both at baseline and in response to arginine or an isonitrogenous mixed amino acid supplementation. Urea production decreased with gestational age in the embolised animals (13.9 ±  3.1 to 11.2 ±  3.0 μmol/kg per min, P ≤ 0.05) but not in the controls (13.3 ±  3.5 to 14.8 ±  6.0 μmol/kg per min). Arginine supplementation increased urea production in both groups, but only at 126 days of gestation (control: 15.0 ±  8.5 to 17.0 ±  9.4 μmol/kg per min; embolised: 11.7 ±  3.1 to 14.3 ±  3.1 μmol/kg per min, P ≤ 0.05). Embolisation reduced foetal arginine concentrations by 20% ( P ≤ 0.05) while foetal arginine consumption was reduced by 27% ( P ≤ 0.05). The proportions of plasma citrulline and hydroxyproline derived from arginine were reduced in the embolised animals. These data suggest that foetal urea production and arginine metabolism are perturbed in late gestation after placental embolisation.

Background and Purpose: In the early 1980s, diagnosing periventricular leukomalacia (PVL) in neonates by using cranial sonography was possible for the first time. Our purpose was to investigate the possibility of diagnosing PVL in the acute stage by using MR imaging. We evaluated early MR features of hypoxic-ischemic brain injury in neonates with periventricular densities (flares) on cranial sonograms to determine the added value of MR imaging over sonography alone for early diagnosis of brain damage., Methods: In a prospective study, infants who showed flares and/or cysts on sonograms underwent MR imaging during the (sub)acute stage., Results: Fifty infants were classified according to the highest sonographic grade up to the day of MR imaging: 23 infants had sonographic grade 1 (flares < 1 week), 15 had sonographic grade 2 (flares > or = 1 week), four had sonographic grade 3 (small localized cysts), and eight had sonographic grade 4 (extensive periventricular cysts); none had sonographic grade 5 (multicystic leukomalacia) on the day of MR imaging. Overall, the additional information provided by MR imaging (over sonography alone) consisted of the depiction of hemorrhagic lesions in 64% of the infants. Extent and severity of the hemorrhages varied from isolated punctate lesions to extensive hemorrhages throughout the white matter; the latter were followed by cystic degeneration at autopsy in two infants. In nine of the 12 infants with cystic PVL, MR images showed more numerous or more extensive cysts. In addition, in two infants, MR images showed cysts not present on sonograms. In 32% of the infants, MR imaging provided no additional information; in these children, all but one had flares on sonograms whereas MR images showed no abnormalities or a zone of mild periventricular signal change., Conclusion: MR imaging can depict the precise site and extent of hypoxic-ischemic brain injury at an earlier stage and allows a wider differentiation of lesions as compared with sonography alone. Hemorrhagic PVL is considered to be rare, but was present in 64% of our study population.

Background: Currently available preterm formulas with energy contents of 3350 kJ (800 kcal)/L promote weight and length gain at rates at or above intrauterine growth rates but disproportionately increase total body fat., Objective: The objective of this study was to determine whether fat accretion in formula-fed, very-low-birth-weight (VLBW) infants could be decreased and net protein gain maintained by reducing energy intakes from 502 kJ (80 kcal)*kg(-)(1)*d(-)(1) [normal-energy (NE) formula] to 419 kJ (100 kcal)*kg(-)(1)*d(-)(1) [low-energy (LE) formula] while providing similar protein intakes (3.3 g*kg(-)(1)*d(-)(1))., Design: The study was a randomized, controlled trial enrolling 20 appropriate-for-gestational-age (AGA) and 16 small-for-gestational-age (SGA) VLBW infants (mean birth weight: 1.1 kg; mean gestational age: 31 wk); energy expenditure and nutrient balance were measured at 4 wk of age and anthropometric measurements were made when infants weighed 2 kg., Results: The percentage of fat in newly formed tissue was significantly lower in AGA infants fed the LE formula (n = 9) than in those fed the NE formula (n = 10) (9% compared with 23%; analysis of variance, P = 0.001). Energy expenditure was higher in AGA infants fed the NE formula than in those fed the LE formula. Skinfold thickness was markedly lower in AGA infants fed the LE formula than in those fed the NE formula, resulting in a lower estimated percentage body fat (8.0 +/- 1.9% and 10.8 +/- 3.5%, respectively; P < 0.05). Three of 6 SGA infants fed the LE formula were excluded during the study because of poor weight gain., Conclusions: Body composition can easily be altered by changing the energy intakes of formula-fed VLBW infants. Energy intakes in these infants should be >419 kJ (100 kcal)*kg(-)(1)*d(-)(1).

The effect of the route of nutrient administration on the relative rates of leucine and phenylalanine kinetics was examined in 30 low birth weight (LBW) infants using L-[1-(13)C]leucine, L-[2H5]phenylalanine, and L-[2H2]tyrosine tracers. The infants received special premature formula (PF, n = 10, 117 +/- 8 kcal.kg-1.d-1 and 3.2 +/- 0.2 g protein.kg-1.d-1) or fortified human milk (HM, n = 10, 106 +/- 6 kcal.kg-1.d-1 and 3.0 +/- 0.2 g protein.kg-1.d-1), or parenteral nutrition (PN, n = 10, 80 +/- 25 kcal.kg-1.d-1 and 1.8 +/- 0.3 g protein.kg-1.d-1). The rate of appearance (Ra) of leucine (RaLeu), was significantly higher in group PF as compared with groups HM and PN (434 +/- 51 versus 377 +/- 33 and 359 +/- 50 mumol.kg-1.h-1, p < 0.05). The Ra of phenylalanine (RaPhe) was lower in group HM as compared with group PF (94 +/- 18 versus 115 +/- 16, p < 0.05), RaPhe in group PN (108 +/- 24 mumol.kg-1.h-1) was in between group PF and HM. The relative rate of RaPhe and RaLeu expressed as RaPhe/ RaLeu ratio was lower in all groups than that expected from reported whole body protein composition and from that reported in adults. The ratio of phenylalanine hydroxylation to leucine decarboxylation was 0.202 in group PF, 0.212 in group HM, and 0.161 in group PN, suggesting a higher rate of decarboxylation of leucine relative to hydroxylation of phenylalanine. We conclude that: 1) the higher RaLeu compared with the RaPhe may be the result of either a higher turnover of a body protein enriched in leucine or the consequence of higher leucine intake in infant nutrition and 2) whole body protein kinetics calculated from a single amino acid tracer do not adequately represent whole body protein metabolism.

Previously, we found evidence that bisferiens peaks in the radial artery pressure wave in the newborn infant may suggest the presence of a left-to-right shunt through a patent ductus arteriosus (PDA). The purpose of the present study was to analyze the origin of this pulsus bisferiens. Starting from the assumption that the radial artery pressure wave form is similar to the aortic pressure wave form, as described previously, we attempted to explain the bisferiens peaks on the basis of echocardiographically obtained ascending aortic flow. We studied 11 preterm mechanically ventilated infants with a left-to-right shunt through a PDA and 7 without. Aortic volume flow was established echocardiographically, and radial artery blood pressure measurement was performed with a high fidelity cathetermanometer system. Ascending aortic peak flow during PDA was significantly higher in the case of PDA, compared with the case without PDA. An augmented peak flow with an abrupt decline after the high peak in PDA, resulting in a sharp pressure peak with a steep decline after the peak, was thought to explain the first sharp peak of pulsus bisferiens. An abrupt decline of flow after peak flow is thought to be due to the fast runoff of blood through the ductus. According to the pulsatile pressure dynamics theories, which state that pressure wave forms consist of forward and backward wave forms, the second peak of the pulsus bisferiens can be explained by the return of the reflected (backward) wave form when the forward wave form has already considerably decreased. We conclude that the bisferiens peaks found in PDA result from a combination of large stroke volume (augmented first peak) and large runoff (quick decline of the forward wave) before the return of the reflected wave.

Previously, we found evidence that radial artery pressure wave forms in newborns represent central aortic wave forms, provided that pressure is measured with adequate accuracy. Therefore, we postulated that the neonatal radial artery wave form, like the adult aortic wave form, may contribute to cardiovascular diagnosis. We investigated whether radial artery wave forms in infants suffering from patent ductus arteriosus (PDA) are different from the wave forms as seen without the presence of PDA. We studied 34 newborn infants with a radial artery line and with the possible clinical diagnosis of PDA with left-to-right shunt. On the basis of echocardiographic examination to assess PDA, these infants were divided in two groups: infants with PDA (n = 24) and without PDA (n = 10). In 15 out of 24 infants with PDA, recordings were repeated after ductal closure. Blood pressure measurement was performed with a high fidelity cathetermanometer system using a tip-transducer (natural frequency 95 Hz, damping coefficient 0.15). Contour analysis was performed by describing morphology of the waves during PDA and without PDA. In 23 out of 24 infants with PDA, a pulsus bisferiens was present: two peaks separated by a deep cleft. The average pressure difference between the first pressure peak and the cleft [delta Ppeak1] was 0.35 +/- 0.19 kPa, and the average difference between the cleft and the second pressure peak [delta Ppeak2] was 0.44 +/- 0.23 kPa. the ratio of mean magnitude of delta Ppeak1 and delta Ppeak2 was 0.81 +/- 0.26. None of the 10 infants without PDA showed pulsus bisferiens.(ABSTRACT TRUNCATED AT 250 WORDS)

During total parenteral nutrition in preterm infants, glucose may be infused at high rates, but it is not known if the endogenous glucose production is fully suppressed under these circumstances. Eight preterm appropriate for gestational age (AGA) (birth wt: 1613 +/- 151 g, gestational age: 31.1 +/- 1.5 wk) and eight preterm small for gestational age (SGA) newborn infants (1185 +/- 241 g, 32.9 +/- 2.6 wk) receiving a glucose infusion rate of 7.55 +/- 0.56 and 8.16 +/- 0.65 mg/kg.min, respectively, were studied during continuous total parenteral nutrition at postnatal d 8. Glucose oxidation rate was determined with a primed constant infusion of [U-13C] glucose, measuring the 13CO2 production in breath gas by isotope ratio mass spectrometry and the glucose production rate in plasma by gas chromatography mass spectrometry. In breath gas of AGA and SGA infants, 60 and 65%, respectively, of the infused tracer appeared as 13CO2. The glucose production rates were 7.97 +/- 1.61 and 8.12 +/- 1.84 mg/kg.min in AGA and SGA infants, respectively, indicating that no significant endogenous glucose production occurred. The glucose oxidation calculated from the glucose production and 13CO2 production was 4.74 +/- 0.99 mg/kg.min in AGA infants and was significantly different from the carbohydrate oxidation rate of 6.62 +/- 1.23 mg/kg.min measured by simultaneous indirect calorimetry. In SGA infants, however, the glucose and carbohydrate oxidation rates were not significantly different at 5.33 +/- 1.56 and 6.16 +/- 2.45 mg/kg.min. It is concluded that 1-wk-old AGA or SGA preterm infants receiving total parenteral nutrition of 80 kcal/kg.d produce no endogenous glucose and their glucose oxidation rates are similar at 63-65% of the glucose infused. It is suggested that the significant difference between glucose and carbohydrate oxidation rates observed in AGA but not in SGA infants is due either to a higher rate of lipogenesis from carbohydrates, or, less likely, to a higher rate of glycogen oxidation.

Medium-chain triglycerides, with a chain length of eight and 10 carbon atoms, form up to 50% of the total fat content in some preterm infant formulas. In 20 small preterm infants (birthwt: 1153 +/- 227 g; mean +/- SD) fed a special formula containing 40% MCT, a primed constant oral infusion study of 1-13C-potassium octanoate was conducted to quantify the oxidation of MCT. A plateau in 13C enrichment in breath CO2 was reached in all patients within 1-3 h. Simultaneously, substrate utilization was measured using a closed system indirect calorimeter. No significant difference was found between appropriate for gestational age (n = 8) and small for gestational age (n = 12) infants in the percentage of the administered tracer that was oxidized (44.9 +/- 9.1% versus 48.5 +/- 11.0%). In all patients, the recovery was calculated to be 47.1 +/- 10.2%, which is less than previously estimated and corresponds to a mean MCT oxidation of 1.26 +/- 0.27 g/kg/d. With indirect calorimetry, a total fat oxidation of 1.42 +/- 0.84 g/kg/d in appropriate for gestational age and 2.00 +/- 0.85 g/kg/d in small for gestational age infants was found, indicating that MCT accounted for around 85% of the total fat oxidation in appropriate for gestational age versus 65% in small for gestational age infants.