Electrophysiological effects of dridocainide on isolated canine, guinea-pig and human cardiac tissues

  title={Electrophysiological effects of dridocainide on isolated canine, guinea-pig and human cardiac tissues},
  author={Csaba Pankucsi and Peter P. Nanasi and M. Heged{\"u}s and Anik{\'o} Kov{\'a}cs and G{\'a}bor Sz{\'e}n{\'a}si and Katalin Szemeredi},
  journal={Naunyn-Schmiedeberg's Archives of Pharmacology},
The cellular electrophysiological effects of dridocainide (EGIS-3966), a novel class I antiarrhythmic agent, was studied using conventional microelectrode techniques in canine cardiac Purkinje fibres and papillary muscle preparations obtained from humans and guinea-pigs. In each preparation, dridocainide (0.6–2 μmol/l) decreased the maximum velocity of action potential upstroke (Vmax) in a frequency-dependent manner, although marked differences were observed in its effects in Purkinje fibre and… 


Effects of procaine amide on the electrophysiologic properties of the canine ventricular conducting system.
The voltage-time course of repolarization was altered in such a way that action potentials dissimilar in duration, recorded from sites proximal to, distal to and at the area of maximum action potential duration became similar.
Concentration- and rate-dependent electrophysiological effects of restacorin on isolated canine purkinje fibres
The results indicate that the cellular electrophysiological effects produced by restacorin in dog cardiac Purkinje fibres best resemble those produced by recognized class Ic antiarrhythmic drugs.
Action potential, membrane currents and force of contraction in mammalian heart muscle fibers treated with quinidine.
  • H. Nawrath
  • Chemistry, Medicine
    The Journal of pharmacology and experimental therapeutics
  • 1981
The results show that the effects of quinidine and the different changes of the action potential configuration can be explained by an unspecific inhibition of the currents of sodium, calcium and potassium.
Reassessment of the electrophysiological effects of the antiarrhythmic agent quinidine in canine purkinje fibers.
The results confirmed the previous findings that quinidine in a dose-related manner suppressed spontaneous activity, prolonged effective refractory period and depressed the maximal rate of upstroke.
Effects of flecainide on the electrophysiologic properties of isolated canine and rabbit myocardial fibers.
The data indicate that the overall electrophysiologic effects of flecainide in isolated cardiac muscle are complex with a major depressant action on Vmax that may account for its dominant antiarrhythmic effects.
The electrophysiological effects of disopyramide phosphate on canine ventricular muscle and Purkinje fibers in normal and low potassium.
  • T. Kus, B. Sasyniuk
  • Chemistry, Medicine
    Canadian journal of physiology and pharmacology
  • 1978
Modifications of the electrophysiological actions of disopyramide by low [K+]o suggest that a therapeutic concentration of dispyramide might have less of an antiarrhythmic effect in the presence of hypokalemia.
Effect of lidocaine on the electrophysiological properties of ventricular muscle and purkinje fibers.
Lidocaine's in vivo antiarrhythmic action is strikingly different from those of quinidine or procaine amide, with progression to bizarre action potential depolarization and inexcitability.
Interval-dependent effects of small antiarrhythmic drugs on excitability of guinea-pig myocardium.
  • K. Courtney
  • Chemistry, Medicine
    Journal of molecular and cellular cardiology
  • 1980
Abstract Myocardial depressant actions of seven antiarrhythmic drugs have been studied in vitro in guinea-pig papillary muscle preparations, using upstroke velocity of action potentials as a measure
Effect of antiarrhythmic drugs on the premature action potential duration in canine cardiac Purkinje fibers.
It is concluded that antiarrhythmic drugs belonging to the same class have different effects on the range of premature APD and that these effects cannot be predicted from the effect of the drug on APDb alone.
Quinidine-induced inhibition of transient outward current in cardiac muscle.
The reduction in the transient outward current can explain the lengthening of action potential and provides new insight into the mechanism of action of quinidine as an antiarrhythmic agent.