Abstract
The effects of kava, a native drink from Oceania, on neuromuscular transmission and muscle contractility have been examined in mouse phrenic nerve-hemidiaphragm and frog sartorius muscle preparations using twitch tension and intracellular recording techniques. The extent of muscle paralysis induced by kava was similar in both directly and indirectly stimulated mouse hemidiaphragms. The neuromuscular blockade produced was poorly reversed by calcium and by neostigmine. Intracellular recordings from frog sartorius muscles showed that kava depressed the amplitude of both miniature end-plate potentials (mepps) and end-plate potentials (epps) but had no effect on the frequency of mepps. Kava greatly prolonged the duration of mepps and epps and also slowed and depressed directly elicited muscle action potentials. It is concluded that kava causes paralysis by mechanisms similar to local anaesthetics.
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