I don't know, but I've found many interesting articles that suggest that the placenta protects the fetus from cocaine exposure. Here are some sample abstracts, which I found through a database called Medline. Yoshie
Authors: Potter S. Klein J. Valiante G. Stack DM. Papageorgiou A. Stott W. Lewis D. Koren G. Zelazo PR. Institution: Department of Psychology and Research Institute, McGill University, Montreal, Canada. Title: Maternal cocaine use without evidence of fetal exposure. Source: Journal of Pediatrics. 125(4):652-4, 1994 Oct. Abstract: We report a case of lack of fetal exposure to cocaine and benzoylecgonine as evidenced by meconium and hair analysis, but exposure to nicotine and its metabolite cotinine, after extensive maternal use of cocaine and nicotine. These data suggest that the mode of maternal use of cocaine and individual differences in placental handling of the drug may protect some fetuses, and highlight the need to address interpatient variability.
Authors: Simone C. Derewlany LO. Oskamp M. Johnson D. Knie B. Koren G. Institution: Division of Clinical Pharmacology and Toxicology, Hospital for Sick Children, Toronto, Ontario, Canada. Title: Acetylcholinesterase and butyrylcholinesterase activity in the human term placenta: implications for fetal cocaine exposure. Source: Journal of Laboratory & Clinical Medicine. 123(3):400-6, 1994 Mar. Abstract: The characterization of the enzymes responsible for drug metabolism in the human placenta is of great importance in determining the possible role the placenta plays in protecting the fetus from potentially fetotoxic drugs. We speculate that the placenta metabolizes cocaine, serving to protect the fetus from the drug's ill effects. Cholinesterase, the principle enzyme that metabolizes cocaine, has been hypothesized to be present yet is not well characterized in the human placenta. The purpose of this study was to quantify human placental acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) activity. Human placentas were obtained from elective cesarean sections, and several lobules were thoroughly perfused with cold buffer to ensure minimal contamination from erythrocyte AChE. Subcellular fractions were then prepared from these lobules by using standard differential centrifugation techniques. Microsomes and cytosol were assayed for AChE and BChE activity by using a spectrophotometric assay. BChE activity was found in the cytosolic fraction of the placental villous tissue, whereas AChE activity was measured in the microsomal fraction. By demonstrating that BChE activity is present in human term placenta we have shown that this organ has the capacity to metabolize cocaine and may therefore serve as a metabolic barrier to fetal exposure to cocaine.
Authors: Simone C. Derewlany LO. Oskamp M. Knie B. Koren G. Institution: Division of Clinical Pharmacology and Toxicology, University of Toronto, Ontario, Canada. Title: Transfer of cocaine and benzoylecgonine across the perfused human placental cotyledon. Source: American Journal of Obstetrics & Gynecology. 170(5 Pt 1):1404-10, 1994 May. Abstract: OBJECTIVE: Our aim was to measure the transfer of cocaine and its major metabolite benzoylecgonine across the human term placenta. STUDY DESIGN: By means of in vitro perfusion of the human term placental cotyledon the transfer of these compounds was measured. RESULTS: The steady-state maternal-to-fetal transfer of cocaine (0.18 +/- 0.05 microgram/ml/min) was significantly greater than benzoylecgonine transfer (0.02 +/- 0.01 microgram/ml/min) (p < 0.05). When the perfused tissue was analyzed 32% +/- 7% of the maternal cocaine dose was retained by the placental tissue, whereas only 12% +/- 12% of the maternal benzoylecgonine dose was retained by the placental compartment. CONCLUSIONS: These results suggest (1) the placenta may serve as a depot for large amounts of cocaine, thus offering some degree of fetal protection after bolus administration; (2) fetal exposure may be prolonged by placental retention and subsequent release of cocaine and benzoylecgonine; and (3) benzoylecgonine does not cross the placenta as readily as does cocaine. Variability in placental handling of cocaine and benzoylecgonine may therefore determine fetal exposure to these agents.
Authors: Shearman LP. Meyer JS. Institution: Department of Psychology, Neuroscience and Behavior Program, Tobin Hall, University of Massachusetts, Amherst, MA 01003-7710, USA. Title: Cocaine up-regulates norepinephrine transporter binding in the rat placenta. Source: European Journal of Pharmacology. 386(1):1-6, 1999 Dec 10. Abstract: We investigated the influence of 3 days of continuous cocaine exposure on norepinephrine transporter binding in the rat placenta. On gestational day 17, pregnant rats were implanted subcutaneously with two cocaine-containing Silastic capsules. There were two control groups, one that received capsules with vehicle only and was pair-fed to the cocaine-treated females, and a second group that was untreated and fed ad libitum. Placentas and fetal brains were harvested and frozen on gestational day 20, and subsequently subjected to saturation analyses for norepinephrine transporter binding using the selective ligand [3H]nisoxetine. There was a marked increase in the density (B(max)) of norepinephrine transporter binding sites in the placentas of the cocaine-treated animals compared to both control groups, but no change in the fetal brain. The mechanism underlying this up-regulation of the placental norepinephrine transporter is not yet known, but it could involve a beta-adrenoceptor- and cAMP-mediated induction of transporter gene expression.
Authors: Morishima HO. Whittington RA. Zhang Y. Cooper TB. Institution: Departments of Anesthesiology, Obstetrics and Gynecology, and Psychiatry, College of Physicians and Surgeons, Columbia University, New York, USA. Title: The disposition of cocaethylene in rat maternal, placental, and fetal compartments. Source: American Journal of Obstetrics & Gynecology. 180(5):1289-96, 1999 May. Abstract: OBJECTIVE: The aim of this project was to examine the disposition of maternally administered cocaethylene in the fetus. STUDY DESIGN: Pregnant rats with long-term catheter placement received an intravenous infusion of cocaethylene during a period of 30 minutes. At either the completion of the infusion or 6 hours after the infusion the fetuses were delivered by hysterotomy. Maternal and fetal blood and major tissue samples were obtained for assays of cocaethylene and its metabolites. RESULTS: Cocaethylene was present in all samples obtained at the end of the infusion, but after 6 hours it was no longer detectable in the maternal and fetal systemic circulations. However, a substantial amount of cocaethylene was still present in the placenta on both the maternal and fetal sides, with the concentration on the maternal side being higher, indicating that the placenta stores cocaethylene. At the end of the infusion benzoylecgonine was found in all samples and the maternal concentrations were higher than the corresponding fetal concentrations. This order was reversed 6 hours after infusion. Extremely high concentrations of cocaethylene and benzoylecgonine were found in the amnion. CONCLUSIONS: These results suggest that the placenta limits the transfer of cocaethylene to the fetus. The high affinity of this compound for extraplacental sites cannot be ignored.
Authors: Bailey B. Morris P. McMartin KI. Klein J. Duhart HM. Gillam MP. Binienda Z. Slikker W. Paule MG. Koren G. Institution: Division of Clinical Pharmacology and Toxicology, The Hospital for Sick Children, Toronto, Ontario, Canada. Title: Transplacental pharmacokinetics of cocaine and benzoylecgonine in plasma and hair of rhesus monkeys. Source: Reproductive Toxicology. 12(5):517-23, 1998 Sep-Oct. Abstract: There is large variability in the rate and extent of fetal damage from cocaine in humans; however, the sources of such variability are not presently known. In order to study the relationship between maternal cocaine pharmacokinetics at the end of pregnancy and maternal or infant cocaine and benzoylecgonine hair concentrations at birth, ten rhesus monkeys were administered cocaine intramuscularly throughout pregnancy. Cocaine and benzoylecgonine hair concentrations were determined at birth and correlated with maternal pharmacokinetics during pregnancy. There were no correlations between either maternal cocaine Cmax or AUC0-infinity and maternal and infant hair cocaine or benzoylecgonine concentrations. There were no significant correlations between maternal hair benzoylecgonine concentrations and either maternal benzoylecgonine AUC0-120 (r = 0.60; P = 0.07) or benzoylecgonine Cmax (r = 0.60; P = 0.07). No correlations existed between infant hair benzoylecgonine concentrations and either maternal benzoylecgonine AUC0-120 (r = 0.30; P = 0.40) or benzoylecgonine Cmax (r = 0.30; P = 0.40). Also, no correlation was found between maternal cocaine dose and maternal or infant cocaine and benzoylecgonine hair concentrations. In comparison to toxicants such as nicotine and carbon monoxide for which there is a good correlation between maternal systemic exposure and neonatal concentrations, the lack of a similar relationship for cocaine is consistent with the role of the placenta in contributing to the variability in the amounts of cocaine reaching the fetus and hence, potentially to the risk of adverse fetal outcome.