ABSTRACT
In recent years, a great deal of attention has been devoted to the chemical form in which cocaine is taken by humans. Only the interaction with ethanol is discussed here because of the common co-abuse of the two drugs and because of the current interest in cocaethylene, the metabolite that forms in the presence of the two drugs. Nevertheless, it bears repeating that cocaine-initiated epinephrine release induces hyperglycemia experimentally and that hyperglycemia in turn may potentially enhance ischemia-reperfusion injury in the brain. It is possible that liver damage, which is not a recognized adverse effect of cocaine abuse for the maternal-fetal unit, could be induced via the mechanism of Cocaine Neurotoxicity During Development by cocaine or cocaethylene. The emphasis on active metabolites, species differences, and the special changes in drug response with pregnancy has increased our understanding of fetal and maternal cocaine pharmacology.
