Prolonged isoflurane exposure in neonatal mice led to increased immediate brain cell degeneration, however, no significant reductions in adult neuronal density or deficits in spontaneous locomotion, spatial learning, or memory function were observed.

In neonatal mice, equipotent doses of the three commonly used inhaled anesthetics demonstrated similar neurotoxic profiles, suggesting that developmental neurotoxicity is a common feature of all three drugs and cannot be avoided by switching to newer agents.

Summary:Detection of cerebral hypoxia-ischemia remains problematic in neonates. Near-infrared spectroscopy, a noninvasive bedside technology has potential, although thresholds for cerebral hypoxia-ischemia have not been defined. This study determined hypoxic-ischemic thresholds for cerebral oxygen saturation (ScO 2 ) in terms of EEG, brain ATP, and lactate concentrations, and compared these values with CBF and sagittal sinus oxygen saturation (SvO 2 ). Sixty anesthetized piglets were equipped with near-infrared spectroscopy, EEG, laser-Doppler flowmetry, and a sagittal sinus catheter. After baseline, ScO 2 levels of less than 20%, 20% to 29%, 30% to 39%, 40% to 49%, 50% to 59%, 60% to 79%, or 80% or greater were recorded for 30 minutes of normoxic normocapnia, hypercapnic hyperoxia, or bilateral carotid occlusion with or without arterial hypoxia. Brain ATP and lactate concentrations were measured biochemically. Logistic and linear regression determined the ScO 2, , CBF, and SvO 2 thresholds for abnormal EEG, ATP, and lactate findings. Baseline ScO 2 was 68 + 5%. The ScO 2 thresholds for increased lactate, minor and major EEG change, and decreased ATP were 44 ± 1%, 42 ± 5%, 37 ± 1%, and 33 ± 1%. The ScO 2 correlated linearly with SvO 2 (r ‫ס‬ 0.98) and CBF (r ‫ס‬ 0.89), with corresponding SvO 2 thresholds of 23%, 20%, 13%, and 8%, and CBF thresholds (% baseline) of 56%, 52%, 42%, and 36%. Thus, cerebral hypoxia-ischemia near-infrared spectroscopy thresholds for functional impairment are ScO 2 33% to 44%, a range that is well below baseline ScO 2 of 68%, suggesting a buffer between normal and dysfunction that also exists for CBF and SvO 2 .

In neonates, neocortical and hippocampal neurons are selectively vulnerable to death after DHCA. Both apoptosis and necrosis contribute to neuronal death, beginning early in reperfusion and continuing for days. These data suggest the need for several neuroprotective strategies tailored to the region and death process, initiated during the operation and continued after the operation.