Chronic prenatal cocaine retards maturation of state and of respiratory patterns in swine.

This study assessed effects of prolonged prenatal cocaine exposure on respiratory pattern and sleep-wake states in a postnatal porcine model. Yucatan miniature sows received 2 mg/kg cocaine intravenously four times daily during 0.66-1.0 gestation. At birth, cocaine-exposed litters were fostered to unexposed paired sows and their litters. Chronically instrumented piglets were studied at 3-9 (young) and 21-31 days (older). Sleep-wake states were determined from electrocorticogram, eye movements, submental electromyogram, and behavior, and respiratory patterns were determined from diaphragmatic and posterior cricoarytenoid electromyograms (EMGdi and EMGpca, respectively). Under baseline conditions, prenatal cocaine 1) increased the number of apneas expressed by silence of EMGdi or EMGpca and prolonged the duration of EMGpca-related apneas at both ages; 2) increased the number of periodic breathing episodes at both ages; 3) increased percent time of active sleep and decreased that of wakefulness at both ages; and 4) increased time in quiet sleep in the older animals, producing in them a sleep-wake distribution similar to that of the young neonates. Whereas the findings in the youngest piglets may have been influenced by persistent systemic cocaine, those in the older preexposed piglets, devoid of systemic cocaine, imply that chronic prenatal cocaine retards the postnatal maturation of state and respiratory pattern.