Ernest Brunton Cady1, Osuke Iwata2, Alan Bainbridge1, John Wyatt2, Nikki Jayne Robertson2
1Medical Physics & Bioengineering, UCLH NHS Foundation Trust, London, United Kingdom; 2Institute for Women's Health, University College London, London, United Kingdom
Phosphoethanolamine concentration ([PE]) is high in neonatal brain. [PE] reduction increases mitochondrial respiration. We aimed to elucidate PE's metabolic role following hypoxia-ischaemia (HI). Thirty-three piglets were studied by 31P MRS (27 HI; 6 controls). For severe cerebral injury [PE]/[exchangeable phosphate pool] fell below controls but later recovered: however, [PE]/[nucleotide triphosphate (NTP; mainly ATP)] was almost constant suggesting strong PE to NTP coupling. In cells stressed after HI reduced [ATP] may inhibit ethanolamine phosphokinase resulting in [PE] reduction and stimulation of ATP generation by surviving mitochondria. High neonatal [PE] may be a factor evolved to counter mammalian cerebral birth trauma.