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

作者信息

Luk'ianenko N G, Bogatskiĭ A V, Savenko T A, Vongaĭ V G, Iaroshchenko I M

出版信息

Biofizika. 1985 May-Jun;30(3):427-30.

PMID:2411299
Abstract

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.

摘要

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