Action of veratrine on human skeletal muscle

Abstract

Four patients with well defined, generalized myasthenia gravis and 25 healthy subjects were studied. Veratridine, cevidine, or an approximately equal mixture of the two (veratrine) were introduced intraarterially. They were studied separately, and in relation to acetylcholine, d-tubocurarine, and neostigmine. Evoked action potentials show that veratridine, cevidine, and veratrine exert a powerful inotropie effect on human nuscle. The effect is marked in patients suffering from myasthenia gravis and is of greater amplitude and duration than that of standard anticholinesterase drugs when injected intraarterially. The drugs affect the contracture phase of the muscle. Veratrine may induce a slight net loss of K. Veratridine is unable to enhance or depress the prompt or late depression of action potentials induced by acetylcholine. A mixture of d-tubocurarine and veratridine acted as curare alone. Neostigmine produced decay in action potentials in healthy control subjects and transient repair in patients with myasthenia gravis. Since the force of contraction is increased, it may have some direct effect on the membrane. Veratrine evoked greater mechanical response than neostigmine in healthy and myasthenie subjects without changing the action potentials of either. It is indicated that the integrated action potential is not a reliable indicator of junetional sucesses or mechanical events following partial or complete membrand. depolarization.