Delayed (“Secondary”) Cerebral Energy Failure after Acute Hypoxia-Ischemia in the Newborn Piglet: Continuous 48-Hour Studies by Phosphorus Magnetic Resonance Spectroscopy (original) (raw)

Pediatric Research volume 36, pages 699–706 (1994)Cite this article

Abstract

ABSTRACT: 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 Po2 3.1 (SD 0.6) kPa]. Mean cerebral phosphocreatine concentration [PCr]/inorganic orthophosphate concentration [Pi] decreased from 1.40 (SD 0.29) to 0.01 (SD 0.02), and nucleotide triphosphate concentration [NTP]/exchangeable phosphate pool concentration [EPP] decreased from 0.19 (SD 0.02) to 0.06 (SD 0.04) (p<0.001 for each decrease). On reperfusion and reoxygenation of the brain, mean [PCr]/[Pi] and [NTP]/[EPP] returned to baseline. Observations continuing for the next 48 h showed that [PCr]/[Pi] again decreased, in spite of normal arterial Po2, mean arterial blood pressure, and blood glucose, to 0.62 (SD 0.61) at 24 h (p<0.01) and 0.49 (SD 0.37) at 48 h (p<0.001). [NTP]/[EPP] also decreased, but to a lesser degree. Intracellular pH remained unchanged. These findings appeared identical with those seen in birth-asphyxiated human infants. No changes in cerebral metabolite concentrations took place in six control piglets. The severity of secondary energy failure, as judged by the lowest [PCr]/[Pi] recorded at 24-48 h, was directly related to the extent of acute energy depletion, obtained as the time integral of reduction in [NTP]/[EPP] (p<0.0001). This animal model of secondary energy failure may prove useful for testing cerebroprotective strategies.

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  1. Departments of Paediatrics, University College London, London, United Kingdom
    Ann Lorek, Y Takei, J S Wyatt, Juliet Penrice, A D Edwards, D Peebles, H Owen-Reece, V Kirkbride, C E Cooper, S C Roth & E O R Reynolds
  2. Medical Physics and Bioengineering, University College London, London, United Kingdom
    E B Cady, Marzena Wylezinska, R F Aldridge & D T Delpy
  3. Biochemistry and Molecular Biology, University College London, London, United Kingdom
    G Brown

Authors

  1. Ann Lorek
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  2. Y Takei
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  3. E B Cady
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  4. J S Wyatt
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  5. Juliet Penrice
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  6. A D Edwards
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  7. D Peebles
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  8. Marzena Wylezinska
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  9. H Owen-Reece
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  10. V Kirkbride
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  11. C E Cooper
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  12. R F Aldridge
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  13. S C Roth
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  14. G Brown
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  15. D T Delpy
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  16. E O R Reynolds
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Lorek, A., Takei, Y., Cady, E. et al. Delayed (“Secondary”) Cerebral Energy Failure after Acute Hypoxia-Ischemia in the Newborn Piglet: Continuous 48-Hour Studies by Phosphorus Magnetic Resonance Spectroscopy.Pediatr Res 36, 699–706 (1994). https://doi.org/10.1203/00006450-199412000-00003

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