Simultaneous cocaine and alcohol use produces enhanced euphoria, compared to either substance alone (Farre et al., 1993). This enhanced effect has been attributed to pharmacokinetic factors, such as more rapid absorption and higher plasma concentrations (up to 30% increase) of cocaine (McCance-Katz et al., 1993). Typically, when cocaine and ethanol use coincide, the normal hydrolysis of cocaine to benzoylecgonine by hepatic carboxyesterase enzymes is inhib ited, allowing higher levels of cocaine to remain in the body. A portion of this cocaine undergoes hepatic microsomal transesterification and is converted to cocaethylene (Andrews, 1997; Jatlow et al., 1991). Cocaethylene has very similar behavioral and toxicological effects to cocaine, but these effects last much longer (cocaethylene's plasma half-life is three to five times that of cocaine; Jatlow et al., 1991). Cocaethylene causes significant sustained increases in heart rate and blood pressure, myocardial infarctions, arrhythmias, and decreases in heart functioning, possibly due its inhibitory effects on potassium channels in the heart (O'Leary, 2002). In addition, cocaethylene is associated with seizures, liver damage, and immune compromise in adults (Andrews, 1997). Additional toxicological aspects, such as the effects on the exocrine pancreas, remain unexplored (Jatlow et al., 1991).
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