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PubMed1991

EO-199, a specific antagonist of antiarrhythmic drugs: assessment by binding experiments and in vivo studies.

EO-199, a demethylated analog of the novel class I antiarrhythmic drug EO-122 was found to antagonize the antiarrhythmic activity of EO-122 and that of procainamide (Class IA). EO-199 did not block significantly the activity of a class IB antiarrhythmic agent, lidocaine. EO-199 also displaced the specific binding of [3H]EO-122 to rat heart membranes similarly to procainamide whereas lidocaine did not. The correlation between binding experiments and pharmacological effects points to a possible subclassification of these drugs; the two chemical analogs EO-199 and EO-122, as well as procainamide (IA) but not lidocaine (IB), compete at the same site or the same state of the sodium channel. The availability of a specific antagonist might be useful for studying the mechanism of action of antiarrhythmic drugs as well as an antidote in cases of antiarrhythmics overdose intoxication.

Animals↗
PubMed2004

Human organic cation transporter 3 mediates the transport of antiarrhythmic drugs.

Antiarrhythmic drugs have been considered to be transported by the organic cation transport system. The purpose of this study was to elucidate the molecular mechanism underlying the transport of antiarrhythmic drugs using cells from the second segment of the proximal tubule (S2) cells of mice expressing human-organic cation transporter 3 (S2 human-OCT3). The antiarrhythmic drugs tested were cibenzoline, disopyramide, lidocaine, mexiletine, phenytoin, pilsicanide, procainamide and quinidine. Human-OCT3 mediated a time- and dose-dependent uptake of quinidine and lidocaine, with Km values of 216 and 139 microM, respectively. Human-OCT3 also mediated the uptake of disopyramide and procainamide but not that of phenytoin. All antiarrhythmic drugs tested inhibited histamine uptake mediated by human-OCT3 in a dose-dependent manner. The IC50 values of antiarrhythmic drugs for human-OCT3 ranged between 0.75 and 656 microM. Kinetic analysis revealed that disopyramide, lidocaine, procainamide and quinidine inhibited histamine uptake mediated by human-OCT3 in a competitive manner. In conclusion, these results suggest that human-OCT3 mediates the transport of antiarrhythmic drugs, which may be the mechanism underlying the distribution and the elimination of these drugs.

Animals↗
PubMed1983

Concordance and discordance of drug responses in atrioventricular reentrant tachycardia.

Whether the results of some drug studies could be used to predict the results of other drug studies was examined during serial electrophysiologic drug testing in patients with sustained atrioventricular reentrant tachycardia. The drugs studied were intravenous propranolol, 0.1 mg/kg; intravenous ouabain, 0.01 mg/kg; the combination of propranolol plus ouabain; intravenous procainamide, 0.75 to 1.5 g; oral quinidine, 1.2 to 2.4 g/day; and oral disopyramide, 0.8 to 1.6 g/day. Response was inability to induce sustained tachycardia after administration of a drug. Responses due to increased anterograde limb refractoriness. Six of 10 patients with response to propranolol plus ouabain versus 0 of 9 patients without response to this combination had response to propranolol alone (p less than 0.01). Seven of 14 patients with response to the combination versus 0 of 9 patients without response to the combination had response to ouabain alone (p less than 0.05). Responses due to increased retrograde limb refractoriness. Eight of 9 patients with response to procainamide versus 2 of 17 patients without response to this drug had response to quinidine (p less than 0.01). There was not a significant relation between response to procainamide and response to disopyramide, or between response to quinidine and response to disopyramide. Anterograde limb versus retrograde limb. There was not a significant relation between response to propranolol plus ouabain and response to any class I drug. In conclusion, there are relations between drug responses during electrophysiologic studies in patients with atrioventricular reentrant tachycardia. Thus, it should be possible to simplify these studies.

Adolescent↗
PubMed2000

Disruption of positive selection of thymocytes causes autoimmunity.

To differentiate into T cells, immature thymocytes must engage, through their antigen-specific T-cell receptor, peptides derived from self proteins presented by cortical epithelial cells in the thymus, a process called positive selection. Despite this requirement for self-recognition during development, mature T cells do not normally show autoreactivity. Mice injected in the thymus with procainamide-hydroxylamine, a metabolite of procainamide, develop autoimmune features resembling drug-induced lupus. Here, we show that when thymocytes undergo positive selection in the presence of procainamide-hydroxylamine, they fail to establish unresponsiveness to low affinity selecting self antigens, resulting in systemic autoimmunity.

Amino Acid Sequence↗
PubMedDate not supplied

Pharmacologic conversion of atrial fibrillation: a systematic review of available evidence.

This report reviews the efficacy of currently available antiarrhythmic agents for conversion of atrial fibrilation (AF) to normal sinus rhythm (NSR). A systematic search of literature in the English language was done on computerized databases, such as MEDLINE, EMBASE, and Current Contents, in reference lists, by manual searching, and in contact with expert informants. Published studies involving humans that described the use of antiarrhythmic therapy for conversion of AF to NSR were considered and only studies that examined the use of agents currently available in the United States were included. Studies exclusively describing antiarrhythmic therapy for conversion of postsurgical AF were excluded. The methodology and results of each trial were assessed and attempts were made to acquire additional information from investigators when needed. Assessment of methodological quality was incorporated into a levels-of-evidence scheme. Eighty-eight trials were included, of which 34 (39%) included a placebo group (level I data). We found in recent-onset AF of less than 7 days, intravenous (i.v.) procainamide, high-dose i.v. or high-dose combination i.v. and oral amiodarone, oral quinidine, oral flecainide, oral propafenone, and high-dose oral amiodarone are more effective than placebo for converting AF to NSR. In recent-onset AF of less than 90 days, i.v. ibutilide is more effective than placebo and i.v. procainamide. In chronic AF, oral dofetilide converts AF to NSR within 72 hours, and oral propafenone and amiodarone are effective after 30 days of therapy. We conclude than for conversion of recent-onset AF of less than 7 days, procainamide may be considered a preferred i.v. agent and propafenone a preferred oral agent. For conversion of recent-onset AF of longer duration (less than 90 days), i.v. ibutilide may be considered a preferred agent. For patients with chronic AF and left ventricular dysfunction, direct current cardioversion is the preferred conversion method. Larger, well-designed randomized controlled trials with clinically important endpoints in specific populations of AF patients are needed.

Amiodarone↗
PubMed1992

Blockade of 2,4-dinitrophenol induced ATP sensitive potassium current in guinea pig ventricular myocytes by class I antiarrhythmic drugs.

OBJECTIVE: The aim was to assess the effects of various antiarrhythmic drugs on 2,4-dinitrophenol (DNP) induced outward current (IDNP), presumably the ATP sensitive K+ current (IK,ATP) of isolated cardiac cells and to discuss mechanisms involved in the hypoglycaemia which occurs in patients on these drugs. METHODS: The quasi-steady state current-voltage relationship from the isolated guinea pig ventricular cells was measured using whole cell voltage clamp techniques with a ramp pulse programme. The effects of seven different antiarrhythmic drugs on IDNP were examined. Action potentials were elicited at a rate of 0.2 Hz by an intracellular current injection. RESULTS: DNP (50 mumol.litre-1) increased the quasi-steady state outward current at potentials positive to about -60 mV. This current (IDNP) was completely inhibited by the subsequent application of glibenclamide (1 mumol.litre-1), thereby suggesting that the IDNP is probably IK,ATP. Cibenzoline (10 mumol.litre-1, class Ia), disopyramide (30 mumol.litre-1, class Ia), and procainamide (100 mumol.litre-1, class Ia) significantly inhibited the IDNP by 95.5(SD 11.3)%, 77.8(21.2)%, and 76.4(23.9)% respectively. Flecainide (class 1c) inhibited the IDNP by 66.9(23.9)% at 10 mumol.litre-1 but not at 2 mumol.litre-1. Mexiletine (30 mumol.litre-1, class Ib), pilsicainide (50 mumol.litre-1, class Ic), and E4031 (10 mumol.litre-1, class III) at concentrations as high as approximately fivefold the clinically effective blood levels, did not suppress IDNP. Except for 10 mumol.litre-1 flecainide, all the concentrations listed above which blocked IDNP were within twofold of the clinical blood concentrations documented to be effective for suppression of arrhythmias. Cibenzoline, disopyramide, and procainamide, but not flecainide, belong to class Ia antiarrhythmic drugs. All these class Ia antiarrhythmic drugs "shortened" the action potential duration of guinea pig ventricular cells, an opposite change to that noted for multicellular preparations, eg, guinea pig papillary muscles. CONCLUSIONS: Class Ia antiarrhythmic drugs (cibenzoline, disopyramide, and procainamide) inhibit IDNP (presumably IK,ATP) in guinea pig ventricular cells within a range of therapeutic concentrations. This inhibitory effect of IK,ATP can probably explain the hypoglycaemia which occurs in some patients receiving these drugs, and the prolongation of the action potential duration alleged to occur in "superfused" papillary muscles.

2,4-Dinitrophenol↗
PubMedDate not supplied

Relative binding of therapeutic drugs by sera of seven mammalian species.

The relative binding of acetaminophen, lidocaine, phenobarbital, procainamide, quinidine, and theophylline to sera of seven mammalian species was studied. Pooled commercial sera from cow, goat, horse, human, pig, rabbit, and sheep were supplemented with 5 and 10 mM concentrations of each drug. For each serum, each drug, and each drug concentration, equilibrium dialysis was performed in duplicate against phosphate buffer (pH 7.4, 0.1 M, 4 degrees C). Percent drug bound to serum was calculated. Phenobarbital demonstrated more than 20% binding to goat, horse, human, and sheep serum at both 5 and 10 mM concentrations; more than 20% binding to bovine serum at a concentration of 10 mM; and more than 20% binding to pig and rabbit serum at 5 mM. Quinidine (studied only at 5mM concentration) bound more than 20% to cow, goat, horse, human, pig, and rabbit serum. In contrast, procainamide at both the 5 and 10 mM concentrations showed no binding to cow, horse, pig, rabbit, or sheep serum. Acetaminophen (studied only at 5 mM concentration), lidocaine, and theophylline demonstrated less than 20% binding to each serum. Acetaminophen at 5 mM did not bind to human serum, and lidocaine at 10 mM did not bind to horse or pig serum. Although some interspecies variation in drug binding to the seven sera was noted, the overall magnitude of binding of each drug to each serum was, for the most part, similar. Phenobarbital and quinidine showed stronger (> 20%) binding; procainamide showed negligible binding; and acetaminophen, lidocaine, and theophylline demonstrated intermediate (< 20%) binding.

Acetaminophen↗
PubMedDate not supplied

Effects of etafenone and antiarrhythmic drugs on Na and Ca channels of guinea pig atrial muscle.

Since Ca-mediated electrophysiological phenomena seem to be important in the generation of various arrhythmias, we quantitatively compared the effects of quinidine, disopyramide, procainamide, lidocaine, propranolol, and etafenone, a new coronary vasodilator with antiarrhythmic properties, on Na and Ca channels in normal and depolarized guinea pig atria. The maximum rate of rise of the normal action potential and the amplitude of the depolarized, Ca-mediated action potential were measured to examine the Na and Ca channel activity, respectively. In both preparations, the contractile force was determined concomitantly in order to establish the role of Ca influx in the inotropic effects of the drugs. All six drugs suppressed the Na channel, the effect being strongest with etafenone, followed in order by quinidine, propranolol, disopyramide, lidocaine, and procainamide. Only quinidine, disopyramide, and propranolol suppressed the Ca channel and only in concentrations higher than those required to block the Na channel. Etafenone and procainamide decreased Ca influx, while lidocaine had no effect on it. The negative inotropic effects of propranolol and disopyramide may be due to decreases in Ca influx, but the order drugs seem to have other mechanisms for their inotropic effects.

Action Potentials↗
PubMedDate not supplied

Effects of commonly used cardioactive drugs on atrial and sinoatrial conduction in man.

Atrial and sinoatrial conduction intervals were measured in patients before and after the intravenous administration of one of four cardioactive drugs: procainamide, atropine, ouabain, and propranolol. Procainamide uniformly prolonged atrial conduction and shortened sinoatrial conduction. Atropine also shortened sinoatrial conduction but did not significantly alter atrial conduction. Ouabain prolonged sinoatrial conduction in patients with normal control sinoatrial conduction intervals and did not affect atrial conduction. Propranolol did not significantly alter sinoartrial conduction and only prolonged interatrial conduction in patients with normal base line atrial conduction intervals. Of the cardioactive drugs tested, only procainamide and propranolol significantly altered the atrial conduction intervals; furthermore, the effects of these cardioactive drugs on sinoatrial conduction were disparate from their effects on atrial conduction.

Adult↗
PubMed1994

Effects of E-4031 on atrial fibrillation threshold in guinea pig atria: comparative study with class I antiarrhythmic drugs.

The effects of E-4031, a new class III antiarrhythmic agent, on atrial fibrillation threshold (AFT), atrial effective refractory period (ERP), and interatrial conduction time (ACT) were investigated in Langendorff-perfused guinea pig hearts; the results were then compared with those of the class I agents disopyramide, procainamide, lidocaine, and flecainide. Whole guinea pig hearts were perfused with Tyrode's solution containing acetylcholine (ACh 3 x 10(-7) M). The three indexes were measured before and after administration of the test drugs, using right atrial extrastimulus and 50-Hz continuous stimulation. Disopyramide, procainamide, and flecainide (> or = 10(-6) M) significantly increased AFT. Although E-4031 (> or = 3 x 10(-6) M) also increased AFT, this effect was less potent than that observed with the other drugs. E-4031 (> or = 10(-6) M) significantly prolonged ERP, and this prolongation was less pronounced than that observed with disopyramide but similar to that observed with procainamide or flecainide. E-4031 did not affect ACT, and the greatest prolongation of ACT was observed with flecainide. Lidocaine had no effect on any of the indexes. These findings suggest that in guinea pig hearts E-4031 exerts an antifibrillatory effect by prolonging atrial ERP alone, but this effect is less pronounced than that observed with class I drugs, because AFT measured by 50-Hz continuous stimulation is influenced by both ERP and ACT.

Acetylcholine↗
PubMed2002

Anti-arrhythmic efficacy of nifekalant hydrochloride, a pure class III anti-arrhythmic agent, in patients with healed myocardial infarction and inducible sustained ventricular tachycardia.

In recent clinical trials, class III anti-arrhythmic drugs were found to reduce arrhythmic deaths in patients after myocardial infarction. The purpose of this study was to assess the electrophysiologic properties and anti-arrhythmic efficacy for inducible sustained ventricular tachycardias (VTs) of the pure class III agent nifekalant hydrochloride (MS-551) in comparison with those of procainamide. Programmed ventricular stimulation of up to three extra stimuli was performed for induction of VTs. Effective refractory period (ERP) of the ischemic zone and normal zone was also measured before and after nifekalant. Nifekalant and procainamide suppressed sustained VT induction in four of 15 patients and in six of 15 patients, respectively (p = NS). Sinus cycle length, PR interval, and QRS duration were not changed, but QT and QTc intervals were significantly increased with nifekalant (p < 0.01). Ventricular ERP also increased, whereas there were no significant differences in the increase of ERP between the ischemic and normal zones. The suppression of VT induction did not correlate with the changes in QT, QTc, and ERP after nifekalant administration. There were no significant differences in induced VT cycle length at baseline study between responders and nonresponders to nifekalant. Reverse use dependence was not apparent on review of electrophysiologic parameters. Neither proarrhythmic events nor hemodynamic disturbances occurred after nifekalant administration. It was concluded that nifekalant could be used safely and showed comparable effectiveness to procainamide for the suppression of VT induction.

Adult↗
PubMed1964

OBSERVATIONS ON THE MODE OF ACTION OF SOME CENTRAL DEPRESSANT DRUGS ON TRANSMISSION THROUGH THE CAT SUPERIOR CERVICAL GANGLION.

Methylpentynol, paraldehyde, amylobarbitone and procainamide blocked transmission through the cat superior cervical ganglion, and antagonized the ganglion-stimulating actions of acetylcholine and carbachol injected intra-arterially to the ganglion. Comparison with the effects of tetraethylammonium indicated that the impaired response to acetylcholine could not wholly account for the failure of transmission, which suggested that an impaired release of transmitter substance was a contributory factor. Methylpentynol, paraldehyde and procainamide also blocked the ganglion-stimulating action of potassium chloride. In contrast, amylobarbitone and pentobarbitone did not block the stimulating action of potassium chloride, but antagonized specifically the actions of acetylcholine and carbachol. The anti-acetylcholine activities of the two barbiturate drugs at this site accord with their relative ganglion-blocking activities. It is concluded that the ganglion-blocking action of methylpentynol, paraldehyde and procainamide arises from a nonspecific depression of both presynaptic and postsynaptic elements in the ganglion, but that barbiturate compounds act more specifically on the acetylcholine receptor.

Acetylcholine↗
PubMed1985

Torsades de pointes due to n-acetylprocainamide.

A 66-year-old female with chronic renal failure received five doses of procainamide and developed marked QT interval prolongation and recurrent episodes of torsades de pointes, which were temporally related to high serum n-acetylprocainamide (NAPA) levels and not to procainamide levels. Repeated hemodialysis was effective in lowering NAPA levels. Torsades de pointes is a potential hazard of NAPA accumulation during procainamide administration to patients with renal insufficiency.

Acecainide↗
PubMed1994

Observations from intraatrial recordings on the termination of electrically induced atrial fibrillation in humans.

BACKGROUND: The circulating wavelet hypothesis suggests that atrial fibrillation could terminate by either progressive fusion or simultaneous block of all wavelets. METHODS: Intraatrial recordings from the right atrial free wall were made during procainamide induced (n = 8) or spontaneous (n = 7) termination of electrically induced atrial fibrillation in 14 patients. Atrial rate, mean magnitude squared coherence, and direction of activation during sequential electrograms were measured. Rate and coherence were calculated from the earliest point within 5 minutes prior to termination as well as from the 4-second interval just prior to termination. RESULTS: Termination was directly to sinus rhythm (13 episodes) or to atrial flutter (2 episodes). For the eight procainamide induced terminations, rate decreased between the first measurement and the measurement just prior to termination, from 443 +/- 127 beats/min to 322 +/- 119 beats/min. For the seven spontaneous terminations, rate also decreased from 373 +/- 119 beats/min to 323 +/- 88 beats/min; however, a slight increase in atrial rate prior to termination was observed in three episodes. No specific patterns of atrial cycle lengths were seen during the final few seconds of fibrillation. No increase in coherence was observed. In seven episodes, recordings were made using orthogonal bipoles in the x, y, and z directions, allowing direction of activation of wavefronts to be measured. Three episodes showed multiple instances where direction of activation remained similar over several electrograms as we have previously reported for chronic fibrillation. However, no such instances precipitated termination in any of the seven episodes. CONCLUSIONS: Atrial fibrillation usually terminates directly to sinus rhythm and does so abruptly and without forewarning. While we and others have previously reported that the rate of atrial fibrillation decreases with procainamide infusion, a decrease in the rate of atrial fibrillation is not required for the rhythm to terminate and consequently may not be a part of the termination process at all. Coherence does not demonstrate a progressive increase in the organization of atrial fibrillation prior to termination. Lack of stabilization in the direction of activation of wavefronts in the final few seconds also fails to support fusion of wavefronts as the mechanism of termination of atrial fibrillation. Simultaneous block of all wavelets is consistent with, but not proven by, our observations.

Adolescent↗
PubMed1996

Drug-induced narrowing of the width of the zone of entrainment as a predictor of the subsequent non-inducibility of reentrant ventricular tachycardia after an additional dose of an antiarrhythmic drug.

BACKGROUND: The efficacy of drugs used to treat inducible monomorphic sustained ventricular tachycardia (VT) has been assessed by investigating their ability to suppress inducibility, but the mechanism of the drug action remains to be determined. OBJECTIVES: To determine electrophysiological variables that predict inducibility, divided doses of class I antiarrhythmic drugs were given and their effects were analysed, particularly the ability of the final dose to suppress inducibility. METHODS: The excitable gap was estimated by the zone of entrainment, which was defined as the difference between the cycle length of VT and the longest paced cycle length that interrupted VT during entrainment of VT with rapid pacing at paced cycle lengths in decrements of 10 ms. The cycle length of VT, the block cycle length, and the zone of entrainment were measured in the drug free state and after intermediate and final doses of procainamide, disopyramide, cibenzoline, and mexiletine. RESULTS: Sustained monomorphic VT with a mean (SD) cycle length of 285 (43) ms was induced in 8 patients. It was entrained and interrupted at the block cycle length of 231 (31) ms. The width of the zone of entrainment was 54 (23) ms. In 8 studies VT was not inducible at final doses of procainamide in 4, cibenzoline in 1, and mexiletine in 3. In another 10 studies (procainamide in 4, disopyramide in 1, cibenzoline in 2, and mexiletine in 3), VT remained inducible at the intermediate dose and at the final dose. The cycle length of VT was prolonged to a similar degree in studies of effective and ineffective drugs, but the cycle length that blocked VT was longer at the intermediate dose of the effective drugs. Consequently, the width of the zone of entrainment was significantly narrowed at the intermediate dose of effective drugs and the width of the zone of entrainment was narrower than when ineffective drugs were given (22 (13) ms v 76 (18) or 75 (37) ms at the intermediate and final doses respectively (P < 0.02). CONCLUSION: Drugs that narrowed the zone of entrainment were associated with non-inducibility of VT after the final dose of the drug was given. The baseline variables did not predict the responses to class I antiarrhythmic drugs.

Adult↗
PubMed2003

Spatiotemporal dynamics of reentrant ventricular tachycardias in canine myocardial infarction: pharmacological modulation.

During the transition from a slow to rapid depolarization rhythm, rate-dependent sodium channel blockade develops progressively and increases from beat to beat under procainamide but more abruptly under lidocaine. We investigated the consequences of such differences on the dynamic course and stability of reentrant tachycardias at their onset. Procainamide and lidocaine were infused to equipotent plasma concentrations in canines with three-day-old myocardial infarction. We measured the activation times (ms) and maximum slopes of negative deflections in activation complexes (absolute value: /-dV/dt(max)/ in mV/ms) in 191 unipolar electrograms recorded from ischemically damaged subepicardial muscle during programmed stimulation inducing reentrant tachycardias. Procainamide caused a greater reduction in /-dV/dt(max)/ than did lidocaine in the responses to basic stimulation, and it favored the occurrence of cycle length prolongation at tachycardia onset as the /-dV/dt(max)/ decreased progressively in successive beats. This resulted in conduction block and tachycardia termination in three of eight preparations. In contrast, lidocaine caused a greater depression in /-dV/dt(max)/ in response to closely coupled extrastimuli, but /-dV/dt(max)/ remained constant or even improved thereafter, and none of the tachycardias terminated spontaneously under lidocaine (n = 9). However, the reentrant circuits remained spatially unstable, and lidocaine favored the occurrence of cycle length dynamics displaying constant or decreasing trends. This study supports the notion that cycle length dynamics at tachycardia onset are determined by the properties of the reentrant substrate and their pharmacological modulation.

Animals↗
PubMed1982

Heterogeneity of organic base secretion by proximal tubules.

Rabbit renal tubules were perfused in vitro to characterize the secretion of the organic base procainamide by proximal tubules. When [3H]-procainamide was added to the bath it was secreted into the tubule lumen. In tubules from superficial nephrons secretory rates were greatest in S1, intermediate in S2, and lowest in S3 segments. In juxtamedullary tubules secretory rates were greatest in S1 and S2 and lowest in S3 segments. Secretory rates of p-aminohippurate were greatest in S2 and lowest in S1 and S3 segments of both superficial and juxtamedullary nephrons. The results indicate that there is both axial and internephronal heterogeneity for the secretion of this organic base by rabbit proximal tubules. The segmental secretion of procainamide differs from that of p-aminohippurate.

Aminohippuric Acids↗
PubMed1982

Effect of antidysrhythmic drugs on the heart rate and blood pressure response to treadmill exercise.

The heart rate and blood pressure response to exercise are clinically important parameters evaluated during treadmill testing. These responses may be altered by cardiac drugs. We evaluated the effect of procainamide and disopyramide on the heart rate and blood pressure response to treadmill exercise in 9 healthy volunteers. Each subject performed one Bruce protocol treadmill test while on each of three treatments: placebo, procainamide 1.0 g t.i.d.; disopyramide 150 mg t.i.d. The order of the treatments was randomized in a Latin square design. The study was conducted double-blind. The drugs slightly increased the resting heart rate, but had no significant effect on exercising heart rate or blood pressure. We conclude that the use of procainamide or disopyramide does not interfere with the interpretation of results of treadmill testing.

Adult↗