Phosphorus (31P) spectra from the brains of severely birth-asphyxiated human infants are commonly normal on the first day of life. Later, cerebral energy failure develops, which carries a serious prognosis. The main purpose of this study was to test the hypothesis that this delayed ("secondary'') energy failure could be reproduced in the newborn piglet after a severe acute reversed cerebral hypoxicischemic insult. Twelve piglets were subjected to temporary occlusion of the common carotid arteries and hypoxemia [mean arterial Po, 3.1 (SD 0.6) magnetic resonance spectra from the brains of gas exchange ("birth asphyxia") were commonly normal babies with evidence of critically impaired intrapartum o n the first day of life (1,2). Subsequently, impairment of cerebral energy metabolism developed in some of the Received February 8, 1994; accepted JUIY 7, 1994.

Brain temperature may be important for investigating pathology and cerebroprotective effects of pharmaceuticals and hypothermia. Two methods for estimating temperature using 1H magnetic resonance spectroscopy are described: a partially water-suppressed binomial sequence and non-water-suppressed point-resolved spectroscopy. Relative to N-acetylaspartate (Naa), water chemical shift (delta H2O-Naa) in piglet brain depended linearly on temperature from 30 degrees to 40 degrees C: temperature was 286.9-94.0 delta H2O-Naa degrees C. Thalamic temperature in six normal infants was 38.1 degrees +/- 0.4 degree C indicating that local brain temperature could be estimated with adequate sensitivity for studying pathologic and therapeutic changes.

Severely birth-asphyxiated human infants develop delayed ("secondary") cerebral energy failure, which carries a poor prognosis, during the first few days of life. This study tested the hypothesis that mild hypothermia after severe transient cerebral hypoxia-ischemia decreases the severity of delayed energy failure in the newborn piglet. Six piglets underwent temporary occlusion of the common carotid arteries and hypoxemia. Resuscitation was started when cerebral [phosphocreatine (pCr)]! [inorganic phosphate (Pi)] as determined by phosphorus magnetic resonance spectroscopy had fallen almost to zero and [nucleotide triphosphate (NTP)]![exchangeable phosphate pool (EPP)] had fallen below about 30% of baseline. Rectal and tympanic temperatures were then reduced to 35°C for 12 h after which normothermia (38.5°C) was resumed. Spectroscopy results over the next 64 h were compared with previously established data from 12 piglets similarly subjected to transient cerebral hypoxia-ischemia, but maintained normothermic, and six sham-operated controls.The took place up to 64 h in the hypothermic piglets. We conclude that mild hypothermia after a severe acute cerebral hypoxicischemic insult ameliorated delayed energy failure. (Pediatr Res 37: 667-670, 1995) Abbreviations EPP, exchangeable phosphate pool MABP, mean arterial blood pressure NTP, nucleotide triphosphate 31p MRS, phosphorus magnetic resonance spectroscopy PCr, phosphocreatine Pi, inorganic orthophosphate cellular pH, arterial P0 2 , MABP, and blood glucose concentration , was termed "delayed" or "secondary" energy failure, on the presumption that it was initiated by a preceding "primary" episode of energy imp airment occurring before birth which had resolved with resuscitation. The severity of secondary energy failure is closely related to the chances of death or severe neurodevelopmental disability and microcephaly (1).If the primary insult cannot be avoided by appropriate obstetric interventions, then it may be possible to interrupt the progression to secondary energy failure and its associated delayed neuronal death (2) . One approach is to induce hypothermia. Deep hypothermia during hypoxia-ischemia is 667

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