Chronic prenatal cocaine retards maturation of state and of
respiratory patterns in swine.
Moss, I. R., and A. Laferri[grave]ere.
Developmental Respiratory Laboratory, McGill University, Department
of Pediatrics and Montreal Children's Hospital Research Institute,
Montreal, Quebec, Canada H3H 1P3
APStracts 2:0149A, 1995.
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 iv 4 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 to 9 (young) and
21 to 31 days (older). Sleep-wake states were determined from
electrocorticogram, eye movements, submental electromyogram and
behavior, and respiratory patterns from diaphragmatic and posterior
cricoarytenoid electromyograms (EMGdi, 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.
Received 9 September 1994; accepted in final form 5 April 1995.
APS Manuscript Number A947-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 19 April 1995.