In animal models, exposure to cigarette smoke or nicotine
during fetal development alters the expression of the nicotinic acetylcholine receptor in areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters
fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem
during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine
levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDS.