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Transient perinatal hypoxia-ischemia (HI) can lead to delayed cerebral damage beginning 8-24 h after resuscitation. Cerebroprotective therapies applied soon after HI may thus reduce the severity of brain injury. We have previously shown that MgSO4 administration to newborn piglets after HI fails to prevent the delayed global impairment in cerebral energy metabolism characteristic of severe brain damage. However, high extracellular concentrations of magnesium ions have been found to prevent specific excitotoxic neural cell death in vivo and in vitro. This study therefore examined the hypothesis that MgSO4 administration after HI reduces damage in some regions of the brain even though global energy metabolism is unaffected. Twelve newborn piglets were subjected to global cerebral HI by transient occlusion of both common carotid arteries and reduction of the inspired oxygen fraction to 0.12 until cerebral high-energy phosphates, measured by magnetic resonance spectroscopy, were significantly depleted. Subjects were randomly assigned to two groups of six: the first received MgSO4 (three doses, 400 mg/kg 1 h after resuscitation and 200 mg/kg at 12 and 24 h), and the second received placebo infusions. At 48 h after the start of the experiment, the piglets were killed and their brains were perfused, fixed, and embedded in paraffin wax. Five-micrometer sections were stained with hematoxylin and eosin to allow semiquantitative analysis of the severity and extent of injury to the hippocampus, cerebellum, cerebral cortex, caudate nucleus, thalamus, and striatum and the white matter tracts. There was no difference in the severity of tissue damage between the MgSO4-treated group and the placebo-treated animals in any brain region.

134 CEREBRAL LACTATE AND N-ACETYLASPARTATE/CHOLINE RATIOS AND DELAYED ENERGY FAILURE FOLLOWING ACUTE HYPOXIA-ISCHAEMIA IN THE NEWBORN PIG

The aims of this study were to define 1H metabolite peak area ratios in normal infants and to investigate abnormalities after perinatal asphyxia. The normal infants (n=14) were studied at a gestational plus postnatal age of 31-41(36) weeks. The asphyxiated infants (n=10) were born at 26-41(37) weeks and studied on a total of 19 occasions aged 0-10(2) days. PRESS spectra were collected at 2.4T (TE 270ms) from 8ml voxels located in the thalamus or occipito-parietal region(O-P). Peak areas for the metabolites N-acetylaspartate (Naa), crcatine+phospocreatinc (Cr), choline (Cho) and lactate (Lac) were measured and ratios (mean(SD)) in the normal infants were as follows: Lactate was detected in all 14 infants, and Lac/Naa was higher in the O-P than in the thalamus(p

Interpretation and significance of PVF seen with ultrasound (US) in the brains of newborn infants remain controversial. To find out if PVF predict adverse neurodevelopment, follow up data for PVF without periventricular haemorrhage were analysed from a prospectively scanned cohort (n=725) of very preterm (

6 HUMAN FETAL CEREBRAL OXYGEN SATURATION (SmcO 2 ) MEASURED DURING LABOUR CAN PREDICT ACID-BASE STATE AT DELIVERY

To investigate the prognostic significance of abnormalities of oxidative phosphorylation, the brains of 61 newborn infants born at 27-42 wk of gestation and suspected of hypoxic-ischemic brain injury were examined by surface-coil phosphorus magnetic resonance spectroscopy. Of these infants, 23 died, and the neurodevelopmental status of the 38 survivors was assessed at 1 y of age. Of the 28 infants whose phosphocreatine/inorganic orthophosphate (PCr/Pi) ratios fell below 95% confidence limits for normal infants, 19 died, and of the nine survivors, seven had serious multiple impairments (sensitivity 74%, specificity 92%, positive predictive value for unfavorable outcome 93%). Of the 12 infants with ATP/total phosphorus ratios below 95% confidence limits 11 died (sensitivity 47%, specificity 97%, positive predictive value 91%). Among the 46 infants with increased cerebral echodensities, PCr/Pi was more likely to be low, and prognosis poor, in infants whose echodensities were diffuse or indicated intraparenchymal hemorrhage than in infants whose echodensities were consistent with periventricular leukomalacia. We conclude that when reduced values for PCr/Pi indicating severely impaired oxidative phosphorylation are found in the brains of infants suspected of hypoxic-ischemic injury, the prognosis for survival without serious multiple impairments is very poor, and that when ATP/total phosphorus is reduced, death is almost inevitable.