Effects of quinidine, procaine amide, and N-propyl-ajmaline on skeletal muscle
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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.
Key wordsAntiarrhythmic Drugs Myotonia Skeletal Muscle
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- Bleifeld, W.: Side effects of antiarrhythmic drugs. Naunyn-Schmiedebergs Arch. Pharmak. 269, 282–291 (1971).Google Scholar
- Boistel, J., Fatt, P.: Membrane permeability change during inhibitory transmitter action in crustacean muscle. J. Physiol. (Lond.) 144, 176–191 (1958).Google Scholar
- Bretag, A. H.: Synthetic interstitial fluid for isolated mammalian tissue. Life Sci. 8, 319–329 (1969).Google Scholar
- Carvalho, A. P.: Calcium-binding properties of sarcoplasmic reticulum as influenced by ATP, caffeine, quinine, and local anesthetics. J. gen. Physiol. 52, 622–642 (1968).Google Scholar
- Kottysch, R.: Behandlungsergebnisse mit N-(n-Propyl)-ajmalinhydrogentartrat. Med. Klin. 64, 156–160 (1969).Google Scholar
- Lipicky, R. J., Bryant, S. H., Salmon, J. H.: Cable parameters, sodium, potassium, chloride and water content, and potassium efflux in isolated external intercostal muscle of normal volunteers and patients with myotonia congenita. J. clin. Invest. 50, 2091–2103 (1971).Google Scholar
- Lüllmann, H.: Das Verhalten der cellulären Potentiale der Herzmuskulatur bei verschiedenen experimentellen “Insuffizienzformen”. Naunyn-Schmiedebergs Arch. exp. Path. Pharmak. 237, 447–458 (1959).Google Scholar
- Munsat, T. L.: Therapy of Myotonia. Neurology (Minneap.) 17, 357–367 (1967).Google Scholar
- Rüdel, R., Senges, J.: Mammalian skeletal muscle: reduced chloride conductance in drug-induced myotonia and induction of myotonia by low-chloride solution. Naunyn-Schmiedeberg's Arch. Pharmacol. 274, 337–347 (1972).Google Scholar
- Sandow, A., Taylor, S. R., Preiser, H.: Role of the action potential in excitationcontraction coupling. Fed. Proc. 24, 1116–1123 (1965).Google Scholar
- Senges, J., Rüdel, R.: Experimental myotonia in mammalian skeletal muscle: changes in contractile properties. Pflügers Arch. 331, 315–323, (1972).Google Scholar
- Senges, J., Rüdel, R., Schmid-Wiedersheim, E.: Effect of sparteine on normal and myotonic mammalian skeletal muscle. Naunyn-Schmiedeberg's Arch. Pharmacol. 274, 348–356 (1972).Google Scholar
- Szekeres, L., Vaughan Williams, E. M.: Antifibrillatory action. J. Physiol. (Lond.) 160, 470–482 (1962).Google Scholar
- Trautwein, W.: Generation and conduction of impulses in the heart as affected by drugs. Pharmacol. Rev. 15, 277–332 (1963).Google Scholar
- Wegehaupt, R., Hager, W.: Behandlung von Herzrhythmusstörungen mit N-Propyl-ajmalin-bitartrat. Dtsch. med. Wschr. 95, 938–942 (1970).Google Scholar
- Weidmann, S.: Effects of calcium ions and local anaesthetics on electrical properties of Purkinje fibres. J. Physiol. (Lond.) 129, 568–582 (1955).Google Scholar
- Wolf, A.: Quinine: An effective form of treatment for myotonia. Arch. Neurol. Psychiat. (Chic.) 36, 382–383 (1936).Google Scholar