Weese-Mayer D E, Barkov G A
Department of Pediatrics, Rush-Presbyterian-St. Luke's Medical Center, Rush Medical College, Rush University, Chicago, Illinois 60612.
Am Rev Respir Dis. 1993 Sep;148(3):589-96. doi: 10.1164/ajrccm/148.3.589.
To investigate the effect of prenatal cocaine on the physiologic responses to hypoxia, we evaluated ventilation, oxyhemoglobin saturation, and pulse rate at 0.21 FIO2 (baseline) and in response to 20-min exposure to either 0.15 or 0.08 FIO2 on Days 4 to 6 of life in 31 unanesthetized New Zealand white rabbit pups born to cocaine-exposed (30 mg/kg/day of subcutaneous cocaine HCl injection from Days 7 to 15 of a 32-day gestation) or free-fed (injection of sterile water) does. We found that baseline ventilation (measured by dual-sidearm pneumotachograph from the plethysmograph), SaO2 (measured by pulse oximeter), and pulse rate did not differ significantly between cocaine-exposed and free-fed pups. At 0.15 FIO2, cocaine-exposed pups had increased VI (p < 0.0005), VT (p < 0.0005), and VT/TI (p < 0.0005) compared with free-fed pups, but no significant difference in f, TI, TE, TI/TT, SaO2, or pulse rate. At 0.08 FIO2, cocaine-exposed pups had increased VI (p = 0.001), VT/TI (p = 0.021), and TE (p = 0.023) compared with free-fed pups, due primarily to the effects in the first 10 min of hypoxic exposure. However, differences in group response were less apparent than at 0.15 FIO2, with a sustained ventilatory response on prolonged exposure to 0.08 FIO2 among free-fed pups but not cocaine-exposed pups. Further, SaO2 (p < 0.0005) and pulse rate (p = 0.012) were significantly lower among cocaine-exposed pups compared with free-fed pups, particularly after 10-min exposure to 0.08 FIO2 when VI was equivalent.(ABSTRACT TRUNCATED AT 250 WORDS)
