Ethanol potentiates the depressant effects of cocaine in human fetal myocardium in vitro.

Abstract

Cocaine and ethanol use is widespread in our society and is not uncommon in pregnant women. Previous work has demonstrated that acute exposure to cocaine produced significant effects on the configuration of human fetal myocardial action potentials and contractility in vitro. It has been hypothesized that these target-specific effects of cocaine may provide a plausible mechanism to account for fetal arrhythmia or sudden fetal death in utero. This study was conducted to determine if treatment with a low concentration of ethanol (200 mg/L) would predispose human fetal myocardium to cocaine-induced toxicity in vitro. Fetal hearts (12-14 weeks) were obtained at the time of elective abortion and transported to the laboratory in cold physiological salt solution. The force of muscle contractions and transmembrane potentials of ventricular walls were studied during external electrical stimulation in a specially constructed superfusion chamber. When a concentration of cocaine (200 micrograms/L physiological salt solution) that singly produced only modest myocardial depression was used in combination with a concentration of ethanol which alone produced nonsignificant changes, marked depression and block of action potentials and contractility resulted. The combined use of ethanol and cocaine produces fetal myocardial depression which is greater than that predicted from the effects of these chemicals individually and may have significant in utero implications.