Prenatal cocaine alters diaphragmatic EMG responses to hypoxia in developing swine.

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.