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Aim: To explore the effects of benactyzine (BEN) on the action potential and contractile force in guinea pig papillary muscles. Methods: Conventional microelectrode technique was used to record the fast action potentials (FAP) and slow action potentials (SAP) of guinea pig papillary muscles. Results: Benactyzine 5, 10, 50 μmol·L -1 suppressed the maximal upstroke velocity ( v max ) of FAP and contractile force (Fc) concentration dependently while prolonged the action potential duration at 50%, 90% repolarization (APD 50 , APD 90 ) and effective refractory period (ERP) of FAP. The suppression on the v max was frequency dependent. Benactyzine 5, 10,50 μmol·L -1 lengthened the APD50, APD90 of SAP induced by isoprenaline or histamine when perfused with KCl 22 mmol·L -1 Tyrode’s solution. The v max of the SAP was not decreased by benactyzine 5, 10 μmol·L -1 but by 50 μmol·L -1 . The effects on the SAP were antagonized by elevation of the extracellular calcium from 2.0 to 5.6 mmol·L -1 . The effects of benactyzine on SAP elicited by tetrodotoxin resembled that by isoprenaline or histamine except the more pronounced suppression on v max and action potential amplitude (APA). The persistent rapid spontaneous activity and triggered tachyarrhythmia induced by ouabain were also abolished immediately by benactyzine 5 μmol·L -1 . Conclusion: Benactyzine can inhibit Na +, K +, Ca 2+ transmembrane movement and intracellular Ca 2+ mobilization in the myocardium, and this may be the electrophysiological basis of its effects against experimental arrhythmias.
Aim: To explore the effects of benactyzine (BEN) on the action potential and contractile force in guinea pig papillary muscles. Methods: Conventional microelectrode technique was used to record the fast action potentials (FAP) and slow action potentials (SAP) of guinea pig papillary muscles. Results: Benactyzine 5, 10, 50 μmol·L -1 suppressed the maximal upstroke velocity (v max) of FAP and contractile force (Fc) concentration dependently while prolonged the action potential duration at 50%, 90% repolarization 50, APD 90) and effective refractory period (ERP) of FAP. The suppression on the v max was frequency dependent. Benactyzine 5, 10, 50 μmol·L -1 lengthened the APD50, APD90 of SAP induced by isoprenaline or histamine when perfused with KCl 22 mmol·L -1 Tyrode’s solution. The v max of the SAP was not decreased by benactyzine 5, 10 μmol·L -1 but by 50 μmol·L -1 The effects on the SAP were antagonized b y elevation of the extracellular calcium from 2.0 to 5.6 mmol·L -1. The effects of benactyzine on SAP elicited by tetrodotoxin resembled that by isoprenaline or histamine except the more pronounced suppression on v max and action potential amplitude (APA). The persistent rapid spontaneous activity and triggered tachyarrhythmia induced by ouabain were also abolished immediately by benactyzine 5 μmol·L -1. Conclusion: Benactyzine can inhibit Na +, K +, Ca 2+ transmembrane movement and intracellular Ca 2+ mobilization in the myocardium, and this may be the electrophysiological basis of its effects against experimental arrhythmias.