Relationship between cerebral interstitial levels of amino acids and phosphorylation potential during secondary energy failure in hypoxic-ischemic newborn piglets.

The aim of this study was to determine the validity of the hypothesis that excitatory amino acids are related to phosphorylation potential during primary and secondary cerebral energy failure observed in asphyxiated infants. We report here the results of experiments using newborn piglets subjected to severe transient cerebral hypoxia-ischemia followed by resuscitation. We examined cerebral energy metabolism by phosphorus nuclear magnetic resonance spectroscopy and changes in levels of amino acid neurotransmitters in the cortex by microdialysis before, during, and up to 24 h after the hypoxic-ischemic insult. The concentrations of aspartate, glutamate, taurine, and gamma-aminobutyric acid were significantly elevated during the hypoxic-ischemic insult compared with prebaseline values. Shortly after resuscitation, glutamate, taurine, and gamma-aminobutyric acid concentrations decreased but then began to increase again. These secondary elevations were greater than the primary elevations. A negative linear correlation was found between primary interstitial levels of glutamate and taurine and minimum values of phosphocreatine/inorganic phosphate during the secondary energy failure. The cerebral energy state depended on the time course of changes in excitatory amino acids, suggesting that amino acids play distinct roles during the early and delayed phases of injury.

Measurement of cerebral oxygenation in neonates after vaginal delivery and cesarean section using full-spectrum near infrared spectroscopy.

To investigate whether or not the mode of delivery produces differences in cerebral oxygenation, cerebral hemoglobin oxygen saturation was measured using full-spectrum near infrared spectroscopy in 26 healthy term newborn infants immediately after birth. Infants in group 1 (n=20) were delivered vaginally, and those in group 2 (n=6) by elective cesarean section. Arterial oxygen saturation in the right hand was also measured simultaneously using a pulse oximeter. Changes in arterial oxygen saturation showed no significant difference between the two groups. The mean+/-S.D. of cerebral hemoglobin oxygen saturation in group 1 increased rapidly after birth, from 29+/-17% at 2 min to 68+/-6% at 8.5 min, followed by an almost constant value (66+/-7% at 15 min). In comparison, cerebral hemoglobin oxygen saturation in group 2 also increased rapidly until 8.5 min, but after this time decreased significantly to 57+/-5% at 15 min after birth. This indicates that the mode of delivery has a marked influence on cerebral oxygenation immediately after birth.