MILD HYPOTHERMIA AFTER SEVERE TRANSIENT HYPOXIA-ISCHEMIA REDUCES THE DELAYED RISE IN CEREBRAL LACTATE IN THE NEWBORN PIGLET

This study tested the hypothesis that mild hypothermia after severe tr ansient hypoxia-ischemia reduces the subsequent delayed rise in cerebr al lactate peak-area ratios as determined by proton (H-1) magnetic res onance spectroscopy (MRS) in the newborn piglet. Nine piglets aged <24 h underwent temporary occlusion of the common carotid arteries and hy poxemia. Resuscitaton was started when cerebral [phosphocreatine]/[ino rganic phosphate] had fallen close to zero and [nucleotide triphosphat e (NTP)]/[exchangeable phosphate pool (EPP)] was below about a third o f baseline. On resuscitation rectal and tympanic temperatures were low ered to 35 degrees C for 12 h after which normothermia (38.5 degrees C ) was resumed. H-1 MRS data collected over 48 or 64 h after resuscitat ion were compared with concurrently established data from 12 piglets s imilarly subjected to transient cerebral hypoxia-ischemia, but maintai ned normothermic, and six sham-operated controls. The severity of the primary insult (judged from the time integral of depletion of [NTP]/[E PP]) was similar in the hypothermic and normothermic groups. The maxim um lactate/N-acetylaspartate ratio observed between 24 and 48 h after resuscitation in the hypothermic group was 0.10 (0.05-0.97), median (i nterquartile range), which was significantly lower than that observed in the normothermic group, 1.28 (0.97-2.14), and not significantly dif ferent from that observed in the control group, 0.08 (0.06-0.11). Simi lar results were obtained for lactate/choline and lactate/total creati ne. We conclude that mild hypothermia after a severe acute cerebral hy poxic-ischemic insult reduces the delayed elevation in lactate peak-ar ea ratios, thus reflecting reduced lactate accumulation.