Decreased ability to arouse in response to hypoxemia and maternal smoking are major risk factors for SIDS. Hypoxic arousal is thought to be mediated by stimulation of peripheral chemoreceptors. In young lambs, acute postnatal nicotine exposure impairs the ventilatory response to acute hypoxia and delays arousal in quiet sleep (QS) (Pediatr Res 39:386A, 1996). The aim of this study was to determine whether prenatal nicotine exposure alters postnatal hypoxic arousal and to ascertain whether this effect is mediated by dopamine.

Subjects & Methods: Eight pregnant ewes were infused continously with nicotine, 40 mg/d during the last trimester. Eight nicotine exposed lambs (N) and 7 control lambs (C) were studied at an age of 3 to 10 d. Hypoxia tests (change in FiO2 to 0.1) were performed in QS during infusion of a) saline, b) domperidone (DP), a DA2 receptor blocker in the peripheral chemoreceptors or c) SCH 23390, a DA1 receptor blocker in the brainstem. Sleep state and arousal were determined by electrophysiologic and clinical criteria.

Results: Arousal was significantly delayed in N compared with C. DP shortened time to arousal significantly in N but not in C. Arousal time was not significantly affected by SCH 23390 in N or in C. Table

Table 1 Time to arousal from onset of hypoxia (s)
Full size table

Conclusion: Prenatal nicotine exposure delays hypoxic arousal from quiet sleep after birth. This effect appears to be mediated by dopaminergic modulation of the peripheral chemoreceptors.