To investigate the effect of prenatal cocaine on the physiologic responses to hypoxia, we evaluated ventilation, oxyhemoglobin saturation, and pulse rate at 0.21 FI(O2) (baseline) and in response to 20-min exposure to either 0.15 or 0.08 FI(O2) 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), Sa(O2) (measured by pulse oximeter), and pulse rate did not differ significantly between cocaine-exposed and free-fed pups. At 0.15 FI(O2), cocaine-exposed pups had increased V̇I (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, Sa(O2), or pulse rate. At 0.08 FI(O2), cocaine-exposed pups had increased V̇I (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 FI(O2), with a sustained ventilatory response on prolonged exposure to 0.08 FI(O2) among free-fed pups but not cocaine-exposed pups. Further, Sa(O2) (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 FI(O2) when V̇I was equivalent. These results suggest that exposure in early gestation to cocaine modifies the ventilatory response to hypoxia, but not baseline ventilation. Further, after prolonged hypoxia, cocaine-exposed pups have more significant oxyhemoglobin desaturation and pulse deceleration despite equivalent V̇I, suggesting that they lack a defense mechanism against prolonged severe hypoxia.
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine