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PubMed1979

Long-term antiarrhythmic therapy with N-acetylprocainamide.

The effects of long-term NAPA therapy were evaluated in 6 patients with chronic PVCs known to respond to this drug during a previous placebo-controlled, dose-ranging trial. Underlying cardiac status was evaluated every six months by switching each patient from NAPA to placebo. Placebo period PVC frequency after one year of NAPA therapy was reduced, compared to baseline placebo values. Mean PEP/LVET, measured while the patients received placebo, was elevated at the beginning of the study but was normal after one year of NAPA therapy. Comparison of NAPA and placebo period observations indicated a reduction in PEP/LVET when NAPA therapy was begun. This effect, however, could not be demonstrated one year later when mean placebo period PEP/LVET was normal. The apparent dependence of this effect on underlying status of left ventricular function suggests that the initial reduction in PEP/LVET represents an an indirect effect of NAPA rather than a direct inotropic action. NAPA therapy was well tolerated by the 6 patients and ANA titers became abnormal in only one, in marked contrast to reported experience with procainamide.

Aged↗

PubMed2004

Antibodies to non-bilayer phospholipid arrangements induce a murine autoimmune disease resembling human lupus.

Antibodies recognizing non-bilayer phospholipid arrangements (NPA) in membrane models and in cell membranes in vivo, triggered an autoimmune-like disease in mice. This exhibited features similar to human lupus and was induced by injecting mice either with the H308 monoclonal antibody specific to NPA, with sera from mice which already had developed the autoimmune disease, or with liposomes treated with the NPA inductors chlorpromazine or procainamide; or with these NPA inductors alone. All these procedures revealed the involvement of antibodies to non-bilayer phospholipids in inducing this autoimmune-like disease. Unraveling the mechanisms of these antibodies might contribute to a better understanding of the molecular and immunological basis of autoimmune diseases like lupus and, hopefully, towards the development of better therapeutic strategies.

Animals↗

PubMed2004

Drug-induced autoantibody formation in mice: triggering by primed CD4+CD25- T cells, prevention by primed CD4+CD25+ T cells.

Although the ability of CD4+CD25+ T suppressor (Ts) cells to prevent experimental autoimmune diseases has been described, nothing is known concerning their role and mechanism of action in xenobiotic-induced autoimmunity. Procainamide, mercuric chloride, and gold(I) are three xenobiotics that can induce autoimmune reactions in humans and rodents. After the induction of IgG1 antinuclear autoantibodies (ANA) in mice treated with either of the above xenobiotics, adoptive transfer of their CD4+CD25+ T cells completely prevented ANA formation in recipients treated with the same xenobiotic; transfer of CD8+ T cells was ineffective. Furthermore, xenobiotic-primed CD4+CD25+ T cells could also partially prevent ANA formation in recipients treated with a different xenobiotic. CD4+CD25- T cells from xenobiotic-treated donors failed to suppress, but induced de novo IgG1 ANA formation in untreated recipients. Our findings suggest that during xenobiotic treatment T cell reactivity may spread from xenobiotic-induced, nucleoprotein-related neoantigens to peptides of the unaltered nucleoproteins.

Animals↗

PubMedDate not supplied

N-acetylprocainamide kinetics during intravenous infusions and subsequent oral doses in patients with coronary artery disease and ventricular arrhythmias.

The kinetics of N-acetylprocainamide (NAPA) were studied in 5 patients (all men, mean age = 62) with coronary artery disease and ventricular arrhythmias during loading infusions of 0.22-0.45 mg/kg/min, prolonged (19-48 hrs) intravenous infusions 2.5-5.2 mg/min, and in 4 of the patients, during subsequent oral doses 1.5-3 g every 8 hrs. Serum, concentrations of NAPA were determined by high-performance liquid chromatography. The individual concentration-time profiles could, with one exception, be described by a two-compartment, open, kinetic model with apparent first-order elimination. The kinetic variables were: initial distribution volume (Vc) 0.20 +/- 0.11 l/kg (mean +/- SD); steady-state distribution volume (Vss) 1.58 +/- 0.55 l/kg; distributional clearance (Cle) 133 +/- 23 ml/(kg X hr); absorption rate constant (Ka) 0.354 +/- 0.173 hr-1; and fraction of dose reaching systemic circulation (F) 1.00 +/- 0.14. The data for one patient who had received increasing oral dosages of 1.5, 2, 2.5 and 3 g every 8 hours resulted in systematic underprediction of observed concentrations at the two highest oral dosing rates. This suggests the possibility of some degree of nonlinearity or time-dependent change in the kinetic behavior of NAPA. Only low concentrations of procainamide, less than 1 mg/L, were found at the end of the infusions.

Acecainide↗

PubMed1975

Azulene analogs of pharmacological agents III: acute toxicity and local anesthetic activity of azulylamides and azulenecarboxamides.

This paper describes the acute toxicity of two azulylamides and six azulenecarboxamides and the nerve conduction-inhibiting properties of some of these compounds. The azulene derivatives are compared to their benzenoid prototypes, lidocaine and procainamide, as part of a continuing investigation of the biological properties of nonbenzenoid aromatic compounds.

Acetamides↗

PubMed1987

Synthesis of 7a-substituted benzoylaminoalkyl-hexahydro-1H-pyrrolizines and evaluation of their antiarrhythmic activity.

Several 7a-substituted benzoylaminoalkyl-hexahydro-1 H-pyrrolizines were synthesized by acylations of 7a-aminoalkyl-hexahydro-1 H-pyrrolizines. All compounds synthesized were evaluated for their antiarrhythmic activities using the chloroform-mouse method, and some of them were found to have significant antiarrhythmic activities, comparable to that of procainamide.

Animals↗

PubMed1990

Schwartz-Jampel syndrome: II. Na+ channel defect causes myotonia.

Skeletal muscle fibers from a patient with Schwartz-Jampel syndrome were studied in vitro. The fibers had normal resting membrane potentials, but their resting [Ca2+]i was elevated. The resting potentials were unstable and spontaneous depolarizations caused twitching in all fibers. Stimulated contractions were characterized by markedly slowed relaxation which was due to electrical after-activity. Neither curare (0.7 microM), tocainide (50 microM), nor phenytoin (80 microM) had an effect on the myotonic activity. In contrast, procainamide (200 microM) suppressed the hyperexcitability without affecting the twitch amplitude. The steady-state current-voltage relation was normal in 5 fibers, but altered in 3 others. These latter fibers had an increased specific membrane resistance owing to a decreased Cl- conductance. The Na+ channels were investigated in the cell-attached patch clamp mode. In all patches on either type of fiber, depolarizing pulses elicited delayed, synchronized openings of Na+ channels. These abnormal openings occurred even after the surface membrane repolarized. We hypothesize that these altered membrane conductances are responsible for the hyperexcitability and the associated slowed relaxation.

Child, Preschool↗

PubMed1996

cDNA cloning and functional expression of a novel rat kidney organic cation transporter, OCT2.

A cDNA encoding a novel organic cation transporter, designated as OCT2 was isolated from the rat kidney. The rat OCT2 cDNA (2,205 bp) had an open reading frame encoding for a 593-amino acid protein (calculated molecular mass of 66 kDa) which shows 67% identity with the rat OCT1. Northern hybridization and reverse transcription-PCR analyses revealed that the rat OCT2 mRNA transcript was expressed predominantly in the kidney, at higher level in the medulla than in the cortex, but this transcript was not detected in the brain, heart, lung, liver, small intestine or spleen. When expressed in Xenopus oocytes, rat OCT2 stimulated the uptake of tetraethylammonium, and the uptake was markedly inhibited by the presence of cimetidine, procainamide and quinidine. These findings suggest that OCT2 is responsible for the transport of cationic drugs in the kidney.

Amino Acid Sequence↗

PubMed1998

Involvement of DNA methylation in binding of a highly repetitive DNA component to nuclear scaffold proteins from rat liver.

Experimental reduction of the amount of CpG methylation in a highly repetitive DNA component was achieved by growth of Ac2F cells in the presence of 5-aza-2'-deoxycytidine or procainamide, as judged by the results of methyl-sensitive restriction endonuclease digestion and colony hybridization. Modification of genomic DNA with these DNA methylation inhibitors increased the release of 370-bp highly repetitive DNA from rat chromosomal DNA by HindIII digestion. This result indicated that highly repetitive DNA components in the nuclear scaffold fraction are hypermethylated. On the other hand, methylated DNA was used for southwestern analysis to investigate the protein(s) which bind specifically to the DNA in the nuclear scaffold fraction. The introduction of additional methylated cytosines within a highly repetitive DNA component affected the binding of DNA to the nuclear scaffold proteins. Thus, cytosine methylation may be involved in the regulation of gene expression and construction of the higher-order structure of chromatin.

Animals↗

PubMed1991

Metabolism of drugs by activated leukocytes: implications for drug-induced lupus and other drug hypersensitivity reactions.

Despite their importance, little is known about the mechanism of idiosyncratic reactions, many such reactions have characteristics that suggest an immune-mediated mechanism. This is particularly true of drug-induced lupus which is an autoimmune syndrome. Certain functional groups are associated with a high incidence of idiosyncratic reactions, probably reflecting the ease with which they are metabolized to reactive metabolites. Although the liver is the principal organ of drug metabolism, most reactive metabolites generated in the liver would not reach other organs in significant concentrations. Because of the function of leukocytes, especially monocytes, in the induction of an immune response, the generation of reactive metabolites by monocytes would seem likely to lead to an immune-mediated adverse reaction. We have found that drugs that are associated with drug-induced lupus are oxidized to reactive metabolites by the myeloperoxidase system of monocytes. The initial step in drug-induced lupus could be haptenization of a protein on the surface of monocytes by these reactive metabolites. Other types of idiosyncratic drug reactions may involve a similar mechanism and the same drugs that induce lupus are usually associated with a high incidence of other types of idiosyncratic reactions. for example, procainamide, which causes the highest incidence of drug-induced lupus, also causes a relatively high incidence of agranulocytosis. Even some of the therapeutic effects of drugs may involve the production of reactive metabolites by myeloperoxidase or thyroid peroxidase.

Antibody Formation↗

PubMed1991

Altered gating and conductance of Na+ channels in hyperkalemic periodic paralysis.

Electrophysiological studies on muscle fibres from patients with hyperkalemic periodic paralysis with myotonia have shown that the episodes of weakness are caused by a sustained depolarization of the sarcolemma to potentials between -40 and -60 mV. In muscle fibre segments from three such patients this sustained depolarization was caused by noninactivating Na+ channels with reduced single-channel conductance blocked by TTX and procainamide. As the chloride conductance was normal, myotonia may be best explained with the abnormal reopenings of the Na+ channels. The recently described genetic linkage between hyperkalemic periodic paralysis with myotonia and the gene coding for the TTX-sensitive Na+ channel suggests an altered primary structure of this channel causing its abnormal function.

Electric Conductivity↗

PubMed1979

Acetylation of phenelzine.

Microsome-free preparations of rodent and human liver were shown to contain N-acetyl transferase from experiments using procainamide as substrate. These preparations then acetylated phenelzine from the quantitative transfer of radiolabeled acetate. This in vitro demonstration of phenelzine acetylation in rodent and human liver was corroborated by the finding of a negative correlation between excretion of phenelzine in urine and sulphadimidine acetylation in 27 patients.

Acetyl Coenzyme A↗

PubMedDate not supplied

Inducible polymorphous ventricular tachycardia following Mustard operation for transposition of the great arteries.

A 22-year-old woman with chronic atrial tachycardia following Mustard's operation for transposition of the great arteries presented with dizziness and ventricular tachycardia documented with dynamic 24-h electrocardiogram. During intracardiac electrophysiology study, programmed ventricular extrastimulation induced polymorphous ventricular tachycardia (torsades de pointes). This was prevented by intravenous administration of procainamide. We postulate that polymorphous ventricular tachycardia is a possible cause of death in patients with Mustard's operation. Postoperative electrophysiologic study may define those patients at risk to develop this potentially fatal arrhythmia.

Adult↗

PubMedDate not supplied

Model parameter estimation and analysis: understanding parametric structure.

We developed three algorithms to facilitate an analysis of the parameter combinations (PASS points) that fit experimental data to a desired degree of accuracy. The clustering algorithm separates PASS points into clusters (PASS clusters) as a preliminary step for the following geometrical parametric analyses. The PASS region reconstruction algorithm defines the space of a PASS cluster to allow further parametric structural analysis. The feasible parameter space expansion algorithm produces a complete PASS cluster to be used for model predictions to evaluate the effects of variability and uncertainty. These algorithms are demonstrated using two pharmacokinetic models; a single compartment model for procainamide and a three-compartment physiologically based model for benzene. We found a more thorough representation of the parameter space than previously considered. Thus, we obtained model predictions that describe better the variability in population responses. In addition, we also parametrically identified a subpopulation that may have a higher risk for cancer.

Algorithms↗

PubMed2005

Antiarrhythmic activity of taurhythman.

Antiarrhythmic properties of taurhythman were demonstrated on experimental models of ventricular (early occlusion and calcium chloride-induced) and atrioventricular (aconitine-induced) arrhythmias. The preparation reduced or prevented episodes of paroxysmal tachycardia and ventricular fibrillation, decreased the incidence of arrhythmias, and increased the lethal dose (LD) of arrhythmogenic agents. By its efficiency, taurhythman was superior to procainamide and comparable to lidocaine.

Aconitine↗

PubMed1982

Evolving concepts of management of stable and potentially lethal arrhythmias.

Recent studies indicate that the eradication of premature ventricular complexes (PVCs) by antiarrhythmic agents is an inadequate end point for estimating long-term protection against potentially lethal arrhythmias. In a study of survivors of prehospital ventricular fibrillation (VF), who have a 30% risk for recurrent VF during the first year of follow-up, we observed an apparent protection against recurrent VF by antiarrhythmic agents even if chronic PVCs were not suppressed by stable therapeutic plasma levels. To expand the data base pertinent to the relationships between PVCs and advanced arrhythmias, we studied six patients with chronic recurrent ventricular tachycardia (VT) and frequent PVCs between episodes of VT. Plasma levels of procainamide (PA) required to protect against recurrent VT averaged 9.4 +/- 3.4 microgram ml, compared with mean levels of 14.9 +/- 3.8 microgram/ml for 85% suppression of PVCs (p less than 0.01). PVC frequency decreased by a mean of only 36% (range -11% to -63%) at plasma levels of PA sufficient to prevent spontaneous VT. Concentration-response relationships between (PA) and PVC suppression were also compared in patients with PVCs during acute myocardial infarction and in patients with PVCs in stable chronic ischemic heart disease. In the former group of patients the mean plasma level of PA required to suppress 85% of the PVCs was 5.0 +/- 0.5 microgram/ml, and in the latter group was 9.3 +/- 0.7 microgram/ml (p less than 0.001). We conclude that the relationship between plasma levels of PA and PVC suppression is different in the two groups of patients, and furthermore, that a high degree of PVC suppression may not be a necessary end point for protecting patients against symptomatic recurrent VT or VF.

Arrhythmias, Cardiac↗

PubMed1983

Electropharmacology of antiarrhythmic drugs.

Cardiac arrhythmias may be caused by abnormalities of impulse initiation, impulse propagation, or a combination of the two. The specific mechanisms that may induce arrhythmias are reviewed, as are the means whereby antiarrhythmic drugs might be expected to modify arrhythmias. The cellular electrophysiologic effects of the following antiarrhythmic drugs are discussed: quinidine, procainamide, disopyramide, lidocaine, tocainide, mexiletine, phenytoin, beta-blocking and slow-channel-blocking drugs, aprindine, bretylium, ethmozin, and amiodarone. A knowledge of the similarities and differences of their actions on the determinants of conduction, on repolarization and refractoriness, on automatic mechanisms, and on afterdepolarizations, when considered in the context of the mechanism of clinically occurring tachyarrhythmias, may provide the correct framework for the choice of an appropriate agent for the control of an individual disorder of rhythm. However, it is emphasized that neither the precise mechanism of various dysrhythmias nor the fundamental basis for the salutary action of antiarrhythmic compounds is completely understood.

Action Potentials↗

PubMed1983

Effect of amiodarone in paroxysmal supraventricular tachycardia with or without Wolff-Parkinson-White syndrome.

In Wolff-Parkinson-White (WPW) syndrome, the two most commonly occurring arrhythmias are circus movement tachycardia (CMT) and atrial fibrillation (AF). In 70% of patients with clinically documented CMT in whom the arrhythmia could be initiated by programmed electrical stimulation of the heart, the same CMT could still be initiated after long-term oral amiodarone administration. Spontaneous clinical recurrence of the arrhythmia was, however, observed in only 10% of patients. This finding suggests that the beneficial effect of amiodarone on CMT is primarily based on the prevention of the CMT-initiating premature beat. This may also apply to atrioventricular nodal reentrant tachycardia, in which amiodarone is also extremely effective in preventing relapses. The role of amiodarone in other forms of reentrant, or ectopic, supraventricular tachycardias is less well defined. During AF in WPW syndrome, the ventricular rate is related to the duration of the anterograde refractory period of the accessory pathway. Amiodarone prolongs this value, resulting in the reduction of ventricular rate during AF. Unfortunately, in the presence of a short anterograde refractory period of the accessory pathway, amiodarone results in only a small amount of lengthening of this value. In these patients the beneficial effect of amiodarone may primarily be related to the prevention of episodes of AF. We also found that the effect of oral amiodarone on the duration of the anterograde refractory period of the accessory pathway can (1) be abolished by sympathetic stimulation with isoproterenol and (2) be predicted from the effect of ajmaline or procainamide given intravenously. These observations clearly have practical clinical implications.

Ajmaline↗