Effect of hyperglycemia on ischemic brain damage during hypothermic circulatory arrest in newborn dogs

The effect of hyperglycemia on ischemic brain damage was investigated in a newborn dog model of hypothermic circulatory arrest. Newborn dogs were anesthetized with halothane, paralyzed, and artificially ventilated to maintain normoxia and acid-base balance. Animals were surface-cooled to 20 degrees C, after which cardiac arrest was effected with i.v. KCl. Before surface cooling, one-half of the dogs (n = 12) received a bolus injection of 50% glucose to increase plasma glucose concentrations to approximately 33 mmol/L (600 mg/dL); control littermates (n = 12) received an equivalent volume of 1 N saline. The dogs remained asystolic for 1.75 h, after which cardiopulmonary resuscitation was accomplished. All animals survived, were allowed to recover from anesthesia at 37 degrees C, and were maintained for 8 h of recovery, at which interval they underwent perfusion-fixation of their brains for pathologic analysis. Histologic grading of brain damage showed no statistically significant difference in the severity of neuronal necrosis within the cerebral cortex or caudate nucleus between hyperglycemic and normoglycemic littermates, with greater brain damage apparent in the amygdaloid nucleus of the hyperglycemic dogs (p < 0.02). Brainstem injury occurred more frequently in the hyperglycemic animals (p < 0.05). Correlation of coefficients analyses revealed a positive correlation between the severity of brain damage and plasma glucose concentration for both the caudate nucleus and amygdaloid nucleus but not for the cerebral cortex. The findings suggest that hyperglycemia superimposed upon hypothermic circulatory arrest in the newborn dog accentuates brain damage only in selected regions of the brain, especially the caudate and amygdaloid nuclei and brainstem, excluding the cerebral cortex.