[Decrease in the fast sodium inflow current, a possible reason for the anti-arrhythmic action of etmozin and mexityl in the late stage of experimental myocardial infarct].
Ethmozine (1--2 mg/kg, i. v.), mexiletine (2--8 mg/kg, i. v.), and tetrodotoxin (TTX) (0.5--3.0 g/kg, i. v.) reduced ventricular arrhythmias occurring 24 hours after ligation of the coronary artery in dogs. Simultaneous infusion of subthreshold doses of ethmozine and TTX or mexiletine and TTX reduced ventricular arrhythmias to the same degree as infusion of threshold doses of either agent alone. TTX, therefore, potentiates the antiarrhythmic effect of ethmozine and mexiletine. Since TTX blocks the fast sodium current specifically, this finding suggests that the antiarrhythmic effect of ethmozine and mexiletine in the late stage of myocardial infarction is due to the inhibition of the fast inward sodium current.
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D005117:Cardiac Complexes, Premature / Q000188:drug therapy; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004353:Drug Evaluation, Preclinical; D004357:Drug Synergism; D005260:Female; D006352:Heart Ventricles / Q000187:drug effects; D007473:Ion Channels / Q000187:drug effects*; D008297:Male; D008801:Mexiletine / Q000627:therapeutic use*; D016293:Moricizine; D009025:Morpholines / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000188:drug therapy*; D010640:Phenothiazines / Q000627:therapeutic use*; D011437:Propylamines / Q000627:therapeutic use*; D012964:Sodium / Q000378:metabolism*; D013779:Tetrodotoxin / Q000627:therapeutic use; D013997:Time Factors
D000889:Anti-Arrhythmia Agents; D007473:Ion Channels; D009025:Morpholines; D010640:Phenothiazines; D011437:Propylamines; D008801:Mexiletine; D016293:Moricizine; D013779:Tetrodotoxin; D012964:Sodium
Umen'shenie bystrogo vkhodiashchego natrievogo toka--vozmozhnaia prichina antiaritmicheskogo deĭstviia étmozina i meksitila v pozdneĭ stadii éksperimental'nogo infarkta miokarda.