Am. J. Respir. Crit. Care Med., Vol 152, No. 6, Dec 1995, 1961-1966.
Prenatal cocaine alters diaphragmatic EMG responses to hypoxia in developing swine
IR Moss, A Laferriere and RE Faltus
McGill University, Department of Pediatrics, Montreal, Quebec, Canada.
To distinguish pure effects of prenatal cocaine exposure on respiratory
control from confounding factors inherent to drug abuse, a porcine model
was established. Cocaine was administered at 2 mg/kg 4 times daily during
0.66-1.0 gestation to 5 paired sows. At birth, cocaine- exposed piglets
were fostered to the unexposed paired sows and their litters. Respiratory
measures were obtained from diaphragmatic electromyographic activity
(EMGDI) of 3 to 9 (young) and 21 to 31 (older) day-old, chronically
instrumented piglets during 10 min each of normoxia and hypoxia (10% O2 in
90% N2), and compared between cocaine- exposed and unexposed animals.
Arterial pH and gas tensions in hypoxia were not altered by cocaine. In the
young neonates, only during hypoxia, cocaine preexposure produced a
transient elevation of the peak and initial slope of the integrated EMGDI
envelope, but did not affect respiratory timing, provided no extensive
periodic breathing or apnea had occurred. In the older animals, during
hypoxia only, cocaine preexposure increased the peak and initial slope of
EMGDI envelope while decreasing summed EMGDI activity, EMGDI duration and
Ttot toward levels seen in the young unexposed neonates. These findings
suggest that prenatal exposure to cocaine retards the normal maturation of
respiratory EMG responses to hypoxia.
