[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.
Luk'ianenko
N G
NG
Bogatskiĭ
A V
AV
Savenko
T A
TA
Vongaĭ
V G
VG
Iaroshchenko
I M
IM
D000157:Aconitine / Q000494:pharmacology*; D031841:Aconitum / Q000031:analogs & derivatives*; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D016275:Atrial Function; D043844:Crown Ethers; D004988:Ethers, Cyclic / Q000494:pharmacology*; D005727:Ganglia, Spinal / Q000187:drug effects / Q000502:physiology; D006168:Guinea Pigs; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects*; D008564:Membrane Potentials / Q000187:drug effects; D009200:Myocardial Contraction / Q000187:drug effects*; D051381:Rats; D012964:Sodium / Q000378:metabolism*
D000889:Anti-Arrhythmia Agents; D043844:Crown Ethers; D004988:Ethers, Cyclic; D007473:Ion Channels; C042148:15-crown-5; C046514:crown lactone I; D012964:Sodium; D000157:Aconitine
Antiaritmicheskaia aktivnost' kraun-laktona I i ego deĭstvie na modifitsirovannye akonitinom natrievye kanaly.