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Effects of lidocaine, procaine, procainamide and quinidine on electrophysiological properties of cultured embryonic chick hearts
Author(s) -
Neto Francisco Riccioppo,
Sperelakis Nicholas
Publication year - 1985
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1985.tb11103.x
Subject(s) - procainamide , procaine , quinidine , lidocaine , chemistry , isoprenaline , electrophysiology , pharmacology , repolarization , propranolol , verapamil , medicine , purkinje fibers , stimulation , anesthesia , endocrinology , calcium
1 The effects of lidocaine, procaine, procainamide and quinidine were studied on organ‐cultured embryonic chick (2–3 day‐old) ventricular cells. 2 Lidocaine (10 −5 − 10 −4 M), in a dose‐dependent manner, reduced the rate of pacemaker discharge, the action potential amplitude (APA), the maximum rate of rise ( V max ) of the upstroke of the action potential and the action potential duration at 50% repolarization (APD 50 ). These changes occurred without alterations in the maximum diastolic potential (MDP). Extracellular electrical field stimulation could still evoke action potentials in cells arrested by 10 −4 M lidocaine, but 10 −3 M lidocaine completely abolished electrical activity. 3 Procaine, procainamide and quinidine, at 5 × 10 −5 M to 10 −3 M, depolarized the cells to around − 30 mV and reduced APA and V max . Procaine and procainamide increased APD 50 , but quinidine shortened it. All the effects described disappeared completely in about 40 min of superfusion with drug‐free Tyrode solution. 4 Isoprenaline (5 × 10 −7 M) and adrenaline (10 −6 M) restored spontaneous firing of preparations arrested by any of the antiarrhythmic agents and repolarized ventricular cells depolarized by procaine, procainamide or quinidine. Propranolol (5 × 10 −7 M) did not affect the depolarization produced by procaine (5 × 10 −4 M), but antagonized its reversal by isoprenaline. 5 In contrast, isoprenaline (10 −6 M) did not produce recovery of automaticity of preparations arrested by verapamil (10 −5 M). 6 Histamine (10 −5 M) or strontium (10 mM) were not able to restore rhythmic activity in cells arrested procaine. 7 Application of long (10–15 s duration) hyperpolarizing currents did not reverse the blocking effect of procaine, procainamide and quinidine. 8 The input resistance increased during the procaine‐induced depolarization. 9 It is suggested that the four agents studied block the slow Na + channels responsible for the upstroke of the action potential in young chick heart cells. A drug‐induced decrease in P K may occur in those cells arrested at low levels of membrane potential.