ANTI-ARRHYTHMIC EFFECTS OF ETHMOZIN IN CARDIAC PURKINJE-FIBERS - SUPPRESSION OF AUTOMATICITY AND ABOLITION OF TRIGGERING

  • 1 January 1983
    • journal article
    • research article
    • Vol. 227  (3) , 578-586
Abstract
The effects of ethmozin were studied on automatic and triggered impulse initiation in isolated canine cardiac Purkinje fibers using standard microelectrode technique. In driven Purkinje fibers with normal (.gtoreq. -80 mV) maximum diastolic potentials, ethmozin (2-4 mg/l or 4.3-8.6 .mu.M) slightly increased the slope of phase 4 depolarization. The rate of normal automatic firing in such fibers was decreased by ethmozin and the threshold (take-off) potential of the pacemaker cells was shifted in the depolarizing direction (toward 0 potential). In fibers treated with BaCl2 (0.10-0.50 mM), abnormal automaticity occurred from maximum diastolic potentials of -38 to -68 mV. Ethmozin (2-4 mg/l) consistently slowed and abolished this abnormal automaticity. This appeared to be associated with a decrease in the rate of diastolic depolarization. When lidocaine, 4 or 10 mg/l (17 or 42 .mu.M), was tested on abnormal automaticity induced by Ba, it decreased the rate of diastolic depolarization and decrease the automatic rate. Lidocaine never terminated Ba-induced abnormal automaticity. Ethmozin also consistently abolished abnormal automaticity in Purkinje fibers taken from the endocardial surface of 24- or 48-h infarct zones. Ethmozin (1-4 mg/l or 2.2-8.6 .mu.M) depressed the amplitude of delayed after depolarizations and terminated triggered activity in Purkinje fibers taken from 24-h infarct zones. Each of these actions could contribute to the antiarrhythmic effects of ethmozin.