[Anti-arrhythmia activity of crown-lactone I and its effect on aconitine-modified sodium channels].

Antiarrhythmic activity of macrocyclic crown-lactone I as well as its effect on biological and model membranes were studied. Crown-lactone displaces the potential dependence of stationary inactivation of TTX-sensible sodium neurons currents towards more negative potentials reducing the modification of those characteristics by aconitine. Proceeding from the comparison between crown-lactone and known antiarrhythmic agents effect on sodium currents a conclusion is made that crown-ethers antiarrhythmic activity cannot be explained by the rhythmoinotropic effect.