Effects of quinidine,procaine amide,and N-propyl-ajmaline on skeletal muscle |
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Authors: | J. Senges R. Rüdel E. Kuhn |
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Affiliation: | (1) Medizinische Poliklinik der Universität Heidelberg, Heibelberg, Germany;(2) Physiologisches Institut der Technischen Universität München, Munich, Germany |
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Abstract: | Summary Membrane and action potentials of rat diaphragm fibres were measured in vitro as affected by quinidine, procaine amide, and N-propyl-ajmaline in concentrations of 10–5 to 10–4 g/ml.All three drugs had immediate effects on the action potential; the effects progressed the faster, the higher the concentration: the de- and repolarization were slowed, the duration increased, the overshoot decreased. Later (e.g., 1 h after application of 10–5 g/ml quinidine) the resting potential started to decrease and the fibres became inexcitable.Electrical threshold was increased and the refractory period was prolonged by all three drugs, most effectively by N-propyl-ajmaline, least by procaine amide. All drugs abolished myotonic symptoms produced by reduction of extracellular chloride.Quinidine and N-propyl-ajmaline (10–5 to 10–4 g/ml) produced a transitory increase of contraction force, on prolonged drug action the muscle went into contracture. Procaine amide always had a negative inotropic effect. All drugs increased contraction time.This work was supported by the Deutsche Forschungsgemeinschaft. |
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Keywords: | Antiarrhythmic Drugs Myotonia Skeletal Muscle |
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