Weese-Mayer D E, Klemka-Walden L M, Barkov G A, Gingras J L
Department of Pediatrics, Rush Medical College, Rush University, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Ill. 60612.
Dev Pharmacol Ther. 1992;18(1-2):116-24.
Recently, investigators have reported an alteration of postnatal respiratory pattern, deficient hypoxic arousal from sleep, and an increased incidence of sudden infant death syndrome (SIDS) among human infants exposed to cocaine prenatally, thus suggesting that prenatal cocaine exposure may perturb the maturation of respiratory control thereby increasing the risk for SIDS. To investigate the effects of prenatal cocaine on postnatal respiration, we evaluated the ventilatory response to 0.21 FIO2 (baseline) and at 0.15, 0.10, and 0.08 FIO2 by the barometric method on days 4-5 of life in 23 New Zealand White rabbit pups born to cocaine-exposed (30 mg/kg/day of cocaine HCl by continuous subcutaneous infusion), pair-fed and free-fed does. The chamber pressure deflection (proportional to VT after appropriate calculation) was computer-sampled at 200 Hz when the unanesthetized pups were resting quietly with no gross body movements. Recording was made after 10 min acclimatization to a specific FIO2. We found that baseline ventilation did not differ significantly among study groups. However, minute ventilation (VI), inspiratory flow (VT/TI), tidal volume (VT), increased significantly with hypoxia to peak values at 0.08 FIO2 in pair-fed and free-fed pups but these measurements did not increase significantly in cocaine-exposed pups. Our finding of a deficient second phase of the hypoxic ventilatory response among cocaine-exposed pups supports the hypothesis that prenatal cocaine perturbs the maturation of respiratory control.(ABSTRACT TRUNCATED AT 250 WORDS)
