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Objectives: To investigate whether a history of maternal tobacco smoking affected the maturation of arousal responses and whether sleeping position and infant age alters these relations. Design: Healthy term infants (13 born to mothers who did not smoke and 11 to mothers who smoked during pregnancy) were studied using daytime polysomnography on three occasions: (a) two to three weeks after birth, (b) two to three months after birth, and (c) five to six months after birth. Multiple measurements of arousal threshold in response to air jet stimulation were made in both active sleep (AS) and quiet sleep (QS) when infants slept both prone and supine. Results: Maternal smoking significantly elevated arousal threshold in QS when infants slept supine at 2-3 months of age (p<0.05). Infants of smoking mothers also had fewer spontaneous arousals from QS at 2-3 months in both prone (p<0.05) and supine (p<0.001) sleeping positions. In infants of non-smoking mothers, arousal thresholds were elevated in the prone position in AS at 2-3 months (p<0.01) and QS at 2-3 weeks (p<0.05) and 2-3 months (p<0.001). Conclusions: Maternal tobacco smoking significantly impairs both stimulus induced and spontaneous arousal from QS when infants sleep in the supine position, at the age when the incidence of sudden infant death syndrome is highest.

Concentrations of the endogenous glutamate receptor antagonist kynurenic acid (KA) were measured in various brain regions and in cisternal cerebrospinal fluid of fetal, newborn, and adult sheep. KA concentrations were significantly higher in the fetal brain and cerebrospinal fluid at 90 and 140 d gestation compared with postnatal ages. In fetuses of 132-139 d gestation, KA concentrations in cerebrospinal fluid collected by drainage from an indwelling cisternal catheter increased significantly after infusion of the organic acid transport inhibitor probenecid (100 or 200 mg/kg, i.v.) indicating active transport of KA out of the fetal brain. In fetuses in which the umbilical circulation had been chronically restricted from 120 to 140 d gestation by partial embolization of the placenta, plasma concentrations of the KA precursor kynurenine were significantly lower than in control fetuses, and KA concentrations in the hypothalamus and hippocampus were significantly reduced; other brain regions were not affected. These results indicate that the production of KA is higher in the fetal brain compared with the newborn and adult brain. Because KA diminishes the risk of excitotoxic neuronal damage under hypoxic-ischemic conditions, the high levels of KA in the brain before birth may have a neuroprotective function. The decrease of KA concentrations in the hypothalamus and hippocampus after umbilical embolization suggests that, after chronic hypoxia in utero, these regions of the brain may become more vulnerable to subsequent episodes of acute hypoxia or ischemia encountered in late gestation or during parturition.

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