title: Mild hypothermia after severe transient hypoxia-ischemia reduces the delayed rise in cerebral lactate in the newborn piglet.
abstract: This study tested the hypothesis that mild hypothermia after severe transient hypoxia-ischemia reduces the subsequent delayed rise in cerebral lactate peak-area ratios as determined by proton (1H) magnetic resonance spectroscopy (MRS) in the newborn piglet. Nine piglets aged < 24 h underwent temporary occlusion of the common carotid arteries and hypoxemia. Resuscitation was started when cerebral [phosphocreatine]/[inorganic phosphate] had fallen close to zero and [nucleotide triphosphate (NTP)]/[exchangeable phosphate pool (EPP)] was below about a third of baseline. On resuscitation rectal and tympanic temperatures were lowered to 35 degrees C for 12 h after which normothermia (38.5 degrees C) was resumed. 1H MRS data collected over 48 or 64 h after resuscitation were compared with concurrently established data from 12 piglets similarly subjected to transient cerebral hypoxia-ischemia, but maintained normothermic, and six sham-operated controls. The severity of the primary insult (judged from the time integral of depletion of [NTP]/[EPP]) was similar in the hypothermic and normothermic groups. The maximum lactate/N-acetylaspartate ratio observed between 24 and 48 h after resuscitation in the hypothermic group was 0.10 (0.05-0.97), median (interquartile range), which was significantly lower than that observed in the normothermic group, 1.28 (0.97-2.14), and not significantly different from that observed in the control group, 0.08 (0.06-0.11). Similar results were obtained for lactate/choline and lactate/total creatine. We conclude that mild hypothermia after a severe acute cerebral hypoxic-ischemic insult reduces the delayed elevation in lactate peak-area ratios, thus reflecting reduced lactate accumulation.
authors.affiliation: Department of Paediatrics, University College London School of Medicine, United Kingdom.
authors.forename: P N
authors.initials: PN
authors.lastname: Amess
authors.forename: J
authors.initials: J
authors.lastname: Penrice
authors.forename: E B
authors.initials: EB
authors.lastname: Cady
authors.forename: A
authors.initials: A
authors.lastname: Lorek
authors.forename: M
authors.initials: M
authors.lastname: Wylezinska
authors.forename: C E
authors.initials: CE
authors.lastname: Cooper
authors.forename: P
authors.initials: P
authors.lastname: D'Souza
authors.forename: L
authors.initials: L
authors.lastname: Tyszczuk
authors.forename: M
authors.initials: M
authors.lastname: Thoresen
authors.forename: A D
authors.initials: AD
authors.lastname: Edwards
authors.forename: J S
authors.initials: JS
authors.lastname: Wyatt
authors.forename: E O
authors.initials: EO
authors.lastname: Reynolds
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000378:metabolism*; D004734:Energy Metabolism; D006859:Hydrogen; D007036:Hypothermia, Induced; D002534:Hypoxia, Brain / Q000378:metabolism* / Q000628:therapy*; D002546:Ischemic Attack, Transient / Q000378:metabolism* / Q000628:therapy*; D007773:Lactates / Q000378:metabolism*; D009682:Magnetic Resonance Spectroscopy; D010710:Phosphates / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D012265:Ribonucleotides / Q000378:metabolism; D013552:Swine
chemical_list: D007773:Lactates; D010710:Phosphates; D012265:Ribonucleotides; D010725:Phosphocreatine; D006859:Hydrogen