The neuroprotective effect of hypothermia instituted after resuscitation from asphyxic cardiac arrest has not been studied in immature brain, particularly in a large animal model with recovery periods greater than 4 d. Moreover, protection from severe hypoxia seen with 3 h of hypothermia was reported to be lost when hypothermic duration was extended to 24 h in unsedated piglets, in contrast to the neuroprotection reported by 72 h of intrauterine head cooling in fetal sheep. Piglets (5-7 postnatal days) were subjected to asphyxic cardiac arrest followed by 24 h of either hypothermia (34°C) or normothermia (38.5-39°C). Comparisons were made with normothermic and hypothermic surgical sham animals without asphyxia, All of these groups were sedated, paralyzed, and mechanically ventilated for the first 24 h to prevent shivering and possible depletion of glucose stores. Hypothermia per se did not cause remarkable structural abnormalities. Ischemic damage was evaluated in putamen at 1 d of recovery without rewarming and at 11 d (10 d ± SD after rewarming). Ischemic cytopathology affected 60 ± 12% of neurons in putamen of normothermic animals compared with 9 ± 6% in hypothermic animals at 1 d of recovery without rewarming. At 11 d of recovery from hypoxia-ischemia, the density of viable neurons (neuron profiles/mm2) in putamen was markedly reduced in normothermic animals (81 ± 40) compared with hypothermic animals (287 ± 22), which was the same as in sham normothermic (271 ± 21), sham hypothermic (288 ± 46) and naïve animals (307 ± 51). These data demonstrate that 24 h of hypothermia at 34°C with sedation and muscle relaxation after asphyxic cardiac arrest prevents necrotic striatal neuronal cell death in immature brain before rewarming, and that the effect is sustained at 11 d after injury without deleterious side effects.
|Original language||English (US)|
|Number of pages||10|
|State||Published - Aug 1 2003|
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health