Abstract □ 144

J.J. Filiano and H.C. Kinney (Biol. Neonate 1994) described a triple-risk model of SIDS. According to this model, SIDS may result from the intersection of three overlaping factors : (i) a critical developmental period, (ii) underlying vulnerability in the infant, and (iii) an exogenous stressor(s). Epidemiological studies on the prevalence of SIDS have identified environmental factors that might be deleterious for fetal and postnatal development. Prenatal events such as maternal smoking or drugs adduction appear to enhance the vulnerability of the developing infant. Disturbances in cardiorespiratory control during sleep have been reported in infants born from mothers who smoked during pregnancy and from substance-abusing mothers. Animal experiments show that fetal exposure to nicotine leads to loss of neonatal hypoxia tolerance. Nicotine administration in newborn animals alters peripheral chemoreceptor sensibility and impairs the ability to autoresuscitation. Chronic prenatal cocaine exposure retards maturation of state and respiration pattern in a postnatal porcine model. Hypoxic stress may enhance the vulnerability of the developing infant. Gestational hypoxia impairs the postnatal development of neural and functional chemoafferent pathways in rats. Neonatal hypoxia has long-term effects with decreased neurochemical activity of the sympathoadrenal system in rats. It has been widely cited that infants with bronchopulmonary dysplasia (BPD) are at risk for SIDS. Delayed postnatal resetting of the peripheral chemoreceptors has been reported in BPD infants. Preventing hypoxemic episodes in BPD infants is probably the most effective means of preventing SIDS. Hopefully, the back-to-sleep campaign has been followed by a dramatic decrease in risk for SIDS. However, prevention of the deleterious effects of environmental stressors such as maternal smoking is still a priority.