3. And simultaneously, in APS Physiology Control of breathing: development session 752.1/board #C483, "Prenatal nicotine exposure does not alter the central ventilatory responsse to serotonin receptor agonists," research by Z. Luo, Costy-Bennett and Fregosi.
Cause of apneas still unknown, but ability to restart breathing remains key
Fregosi said his laboratory wants to better understand how smoking during pregnancy disturbs breathing in infants because of increased rates of asthma, sudden infant death syndrome (SIDS), obstructive sleep apnea and impaired arousal responses during sleep. "Our laboratory is particularly interested in the strong association between maternal smoking on the one hand, and the increased incidence of infantile SIDS and obstructive sleep apnea on the other."
In the current study the team studied how prenatal nicotine exposure affected neonate's ability to respond to decreased levels of blood oxygen, and/or low oxygen combined with elevated carbon dioxide. "This is important when the neonate has an 'apnea,' or cessation of breathing, when they are sleeping, because under these conditions the oxygen can be reduced dramatically. Although we still don't understand the cause of the apneas, we know they are frequent, especially in the early neonatal period.
"This is important physiologically, because a reduced ability to respond to low oxygen and/or high carbon dioxide diminishes the ability of the infant to reinitiate breathing and break the apnea. If the apnea becomes prolonged, the oxygen levels in the blood will drop dramatically leading to cardiovascular arrest and death."
Study used pump implant to simulate prenatal nicotine exposure
The current study exposed animals to nicotine by implanting a small pump loaded with nicotine into pregnant rats, so the neonates were exposed to the nicotine in utero. This mimics the situation observed