Abstract

1. 1. The acute effects of a potent antiarrhythmic agent, amiodarone (AM), were studied in isolated guinea pig ventricular muscle. Transmembrane action potentials were recorded by conventional microelectrode techniques, and isometric contractile tension, by a strain gauge. 2. 2. Short-term (30 min) exposure to 4.4 × 10 −5 M AM did not significantly effect action potential characteristics, whereas the peak developed tension was significantly depressed. 3. 3. On the other hand, long-term (3–5 hr) exposure to the same concentration of AM led to a significant decrease in the resting membrane potential, amplitude of action potential, overshoot of action potential, maximum upstroke velocity of action potential, and the peak developed tention. However, the duration of action potential at all levels of repolarization was not significantly effected by 4.4 × 10 −5 M AM during the entire duration of the experiment. 4. 4. These results suggest that the acute AM's antiarrhythmic actions reported may be not due to APD-lengthening action, but probably due to other actions (mainly, inhibition of Na + channels, Ca 2+ channels).

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