In an in vitro assay on fetal human heart muscle it was demonstrated for the first time that overstimulation by beta-sympathomimetics could cause elective parenchymal necrosis. Fenoterolhydrobromide, which is used for tocolysis on a longterm scale, induces in vitro necroses of individual heart muscle fibers according to a pathogenetic principle postulated by Flekkenstein. The combination of Fenoterolhydrobromide with a Ca++-antagonist prevents elective parenchymal necroses by reducing the Ca++-influx into the heart muscle fibers. These results suggest that elective necroses of heart muscle fibers may be not only of coronarogenic but also of metabolic origin.