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
ABSTRACT. The response of cerebral blood volume (CBVR) to a small induced change in arterial carbon dioxide tension was studied by near-infrared spectroscopy in 17 newborn infants born from 26 wk of gestation to term. All 17 infants were undergoing mechanical ventilation but had apparently normal brains. The CBVR per kPa change in arterial carbon dioxide tension within the range 3.9 to 9.6 kPa was calculated from the change in total cerebral Hb concentration (
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