PRENATAL COCAINE EXPOSURE AND POSTNATAL HYPOXIA INDEPENDENTLY DECREASE CAROTID-BODY DOPAMINE IN NEONATAL RATS

The effects of prenatal cocaine exposure on the levels of carotid body dopamine (DA) and its metabolites 3,4-dihydroxyphenylacetic acid (DOP AC) and homovanillic acid (HVA) were investigated in 5-day-old rat pup s exposed to normoxic and hypoxic conditions. Timed-pregnant Sprague-D awley rats were injected b.i.d. with either cocaine HCl (30 mg/kg) or isotonic saline (1 ml/kg) from gestational days 7-21. On the fifth pos tnatal day, pups were subjected to either 20 min of 0.21 or 0.08 fract ional inspired oxygen (F1O2). Under a strictly timed protocol, both ca rotid bodies were removed from each pup. placed in an antioxidant solu tion to prevent DA breakdown, and subsequently analyzed via HPLC with electrochemical detection to determine carotid body DA and DOPAC conte nt. Two-way ANOVA revealed decreases in DA in cocaine-exposed pups. No HVA was detectable in any of the samples. The 0.08 F1O2 condition dec reased DA compared to 0.21 F1O2. The additive consequences of DA deple tion resulting from the combination of prenatal cocaine and postnatal hypoxia decreased carotid body DA to 14% of control levels, with sever al animals exhibiting DA content below detection limits. Considering t he role of the carotid body in the ventilatory response to hypoxia, th ese data suggest that prenatal cocaine exposure may adversely affect t he normal chemoreceptive function of the carotid body.