Abstract 292 Poster Session II, Sunday, 5/2 (poster 25)

The ability to behaviorally arouse to chemical stimuli during sleep is an important protective response particularly in the young infant. If follows, then, that a dampened arousal response would place an infant at risk of not awakening to sleep related asphyxial events. The relative risk of SIDS is increased in infants whose mothers smoke during pregnancy and in infants exposed to cocaine. We hypothesized that SIDS risk is related to altered respiratory control specifically in the hypoxic arousal response (HAR) during sleep. Thus we measured the ontogeny of the HAR in three groups of infants: cocaine-exposed (Cc), nicotine-exposed (Ni), and controls (Ctl) on postnatal day (d) 6 and at 1.5, 3, and 6 months (m) by modification of the method of Van der Hall, et al. 427 trials on 89 babies were performed. 54 trials were excluded as invalid. Standard statistical methods were performed on 373 valid trials: chi-square, ANOVA, Kruskal Wallis and the Cochran's test; significance being p<0.05. In all groups, the maximal arousal response occurred at 1.5 and 3 m although the pattern of decline was group specific. There were no differences in lowest O2 achieved during the study, O2 at arousal, baseline heart rate, respiratory rate, CO2 or O2. For these preliminary data, arousal to hypoxia did not differ statistically between groups although trends were observed. Arousal was generally associated with complete awakening. However, at 1.5m the Ni exposed infants had fewer awakenings with arousal when compared to the Ctl and the Cc groups (42% Vs 100% Ctl & Cc; p=0.013). This trend was also present in the Cc group at 6d. The most striking finding occurred in the latency or time to arouse. The Ni exposed infants aroused earlier at 6d, 1.5m (33 seconds Vs 93 & 81 seconds) and later at 6m (176 seconds Vs 100 & 97 seconds). Also, more trials were terminated in the exposed groups compared to the Ctl group. These data support the concept that cocaine and nicotine act as respiratory control neuroteratogens. The effects are age and agent specific. Altered arousal to hypoxia in sleep may contribute to SIDS risk.

Co-funded by NIDA and NICHD