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 t imes daily during 0.66-1.0 gestation. At birth, cocaine-exposed litter s were fostered to unexposed paired sows and their litters. Chronicall y instrumented piglets were studied at 3-9 (young) and 21-31 days (old er). Sleep-wake states were determined from electrocorticogram, eye mo vements, submental electromyogram, and behavior, and respiratory patte rns were determined from diaphragmatic and posterior cricoarytenoid el ectromyograms (EMGdi and EMGpca, respectively). Under baseline conditi ons, prenatal cocaine 1) increased the number of apneas expressed by s ilence of EMGdi or EMGpca and prolonged the duration of EMGpca-related apneas at both ages; 2) increased the number of periodic breathing ep isodes at both ages; 3) increased percent time of active sleep and dec reased that of wakefulness at both ages; and 4) increased time in quie t sleep in the older animals, producing in them a sleep-wake distribut ion similar to that of the young neonates. Whereas the findings in the youngest piglets may have been influenced by persistent systemic coca ine, those in the older preexposed piglets, devoid of systemic cocaine , imply that chronic prenatal cocaine retards the postnatal maturation of state and respiratory pattern.