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Antiarrhythmic action of sparteine on direct and indirect models of cardiac fibrillation

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Summary

Papillary muscles from guinea-pig hearts were studied in vitro during exposure to sparteine in concentrations from 10−5 to 10−3 M. Transmembrane voltage was recorded from both electrically driven muscle fibres and preparations with barium-induced fibrillation.

Sparteine produced a large increase in the duration of the effective refractory period which could not be accounted for solely by prolongation of the action potential duration caused by this drug. The membrane responsiveness during the repolarization phase was decreased, and with higher concentrations of sparteine the recovery of excitability following an impulse took much longer than did complete repolarization of the action potential. Conduction velocity and maximum driving rate were reduced.

In spontaneously firing fibers of fibrillating preparations sparteine slowed the rate of depolarization of the pacemeker potential. The maximum diastolic potential was not altered but the threshold potential was markedly decreased. The restoration of suprathreshold excitability after the action potential was much delayed. These drug effects caused most of the spontaneously firing fibers to become latent pacemakers and produced a pronounced reduction of the frequency of propagated electrical activity. The results suggest that the mode of antiarrhythmic action of sparteine is based on partial inhibition of the sodium carrying system at the surface membrane.

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This work was supported by the Deutsche Forschungsgemeinschaft.

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Senges, J., Ehe, L. Antiarrhythmic action of sparteine on direct and indirect models of cardiac fibrillation. Naunyn-Schmiedeberg's Arch. Pharmacol. 280, 265–274 (1973). https://doi.org/10.1007/BF00501351

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  • DOI: https://doi.org/10.1007/BF00501351

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