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- W2059338890 abstract "The effects of SD‐3212 on transmembrane action potentials were examined in right ventricular papillary muscles and in single ventricular myocytes isolated from guinea‐pig hearts. In papillary muscles, SD‐3212 ≥ 3 μ m caused a significant decrease in the maximum upstroke velocity () of action potential without affecting resting membrane potential. The inhibition of was enhanced at higher stimulation frequencies. In the presence of SD‐3212, trains of stimuli at rates ≥ 0.5 Hz led to a use‐dependent inhibition of . The time constant for the recovery of from the use‐dependent block was 1.3 s. Voltage‐dependence of inhibition by SD‐3212 was investigated in single myocytes. The curves relating membrane potential and were shifted by SD‐3212 (10 μ m ) in a hyperpolarizing direction by 6.2 mV. In myocytes treated with SD‐3212 (10 μ m ), the of test action potentials preceded by conditioning clamp to 0 mV was decreased progressively as the clamp pulse duration was prolonged. of test action potentials following a long (1 s) 0 mV clamp recovered at a time constant ranging from 1.01 to 1.22 s, being shorter at the more negative potential within a range from −70 to −90 mV. These findings suggest that the primary electrophysiological effect of SD‐3212 is a use‐ and voltage‐dependent inhibition of sodium channels. From the onset and offset kinetics of the use‐dependent block, SD‐3212 is located between fast and intermediate kinetic Class‐I drugs. From the state‐dependence of sodium channel block, SD‐3212 belongs to inactivated channel blockers." @default.
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- W2059338890 date "1995-01-01" @default.
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- W2059338890 title "Electrophysiological effects of SD-3212, a new antiarrhythmic agent with vasodilator action, on guinea-pig ventricular cells" @default.
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- W2059338890 doi "https://doi.org/10.1111/j.1476-5381.1995.tb13255.x" @default.
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