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PubMed1978

Antiarrhythmic potency of procainamide and N-acetylprocainamide in rabbits.

The antiarrhythmic potency of procainamide (PA) and N-acetylprocainamide (NAPA) has been investigated in rabbits using isolated atrial preparations and ouabain-induced ventricular fibrillation in vivo. At concentrations in the range 3 x 10(-5) to 1 x 10(-3) M, both PA and NAPA decreased the maximum following frequency (MFF) of isolated atria. The dose--response curves were not parallel but at a concentration of 10(-3) M, NAPA had only one tenth of the potency of PA. Threshold level voltage of the atria were increased by PA but NAPA had no significant effect on this parameter. When atria were preincubated with NAPA (1.6 x 10(-4) or 8.0 x 10(-4) M), the dose--response curve for PA on MFF was displaced to the right. Pretreatment of anaesthetised rabbits with either PA (25 mg/kg i.v.) or NAPA (75 mg/kg i.v.) prolonged the time to onset of ouabain-induced ventricular fibrillation. NAPA (25 mg/kg) did not affect the response to PA (25 mg/kg). The data support the view that NAPA is less potent than PA and suggest that, under certain circumstances, NAPA may antagonise the actions of PA.

Animals↗
PubMed1982

Acute coronary artery occlusion-reperfusion-induced arrhythmias in rats, dogs and pigs: antiarrhythmic evaluation of quinidine, procainamide and lidocaine.

Arrhythmias which occur following either abrupt occlusion (CO) of the left anterior descending coronary artery (LAD), or rapid reperfusion (CR) of the same, were studied in rats, dogs and pigs. We found that all rats or pigs exhibited ventricular fibrillation (VF) during CO or after CR in contrast to dogs where more than 30% survived both procedures. In rats, the distribution in the onset of non-lethal arrhythmia or VF appeared to be uniform over the CO period, while in pigs and dogs the onset times clustered into two distinct groups. Also unlike dogs and pigs, the rat frequently (75%) underwent spontaneous defibrillation. Quinidine pretreatment (10 mg/kg i.v.) proved effective in protecting all three species from VF while procainamide (20 mg/kg i.v.) was effective only in rats and dogs. Lidocaine pretreatment (10 mg/kg i.v.) was effective in preventing VF in rats, but increased the incidence of CR-induced VF in dogs and significantly (P less than 0.01) reduced the mean time to VF during CO in pigs. However, lidocaine given immediately after CO in pigs did not reduce the time to VF suggesting that lidocaine given post-infarction would not increase the risk of VF, although the drug appears to be of no therapeutic benefit during the early occlusion period. Similarities in the action of lidocaine in pigs and dogs further suggest that the mechanisms of CR-induced VF in dogs and CO-induced VF in pigs may be similar. These data also support a pivitol role of extracellular K+ accumulation of the production of early post-infarction arrhythmias. Thus, the arrhythmogenic as well as antiarrhythmic properties of the various drugs studied here may relate their known effects on potassium permeability in cell membranes.

Animals↗
PubMed1985

Prolongation of procaine's and procainamide's actions by binding to acryloyl polymers.

Procaine and procainamide were covalently bound to acryloyl monomers and polymers. The dose-response and time-action parameters of the cardiac antiarrhythmic protection afforded by the prototype drugs and their acryloyl derivatives against chloroform-hypoxia-induced cardiac arrhythmias in unanesthetized mice and epinephrine-induced arrhythmias in alpha-chloralose anesthetized cats were determined. Similarly, the pharmacological parameters which characterized their acute toxic responses in unanesthetized male albino mice were also determined. The similar pharmacological spectra of their activity and the parallelism of their lethal dose-response curves indicate that the active constituents of the polymer derivatives are the local anesthetic moieties. Compared to the prototype drugs, the polymer derivatives were more potent on a molar basis and their pharmacological effects were prolonged. The increased potency and duration of action reinforce the idea that the local anesthetic moieties are pharmacologically active while still bound to the polymer backbones.

Acrylic Resins↗
PubMed1985

Efficacy of phenytoin, procainamide, and tocainide in murine genetic myotonia.

A newly described single locus mutation in the mouse, myotonia (mto), features classical myotonia with autosomal recessive inheritance. Phenytoin, procainamide, and tocainide (drugs considered effective in the human myotonias) produced dose-dependent improvement in the behavioral myotonia of mto homozygotes.

Animals↗
PubMed1983

The prevalence of antibodies to histones induced by procainamide in old people, in cancer patients, and in rheumatoid-like disease.

Antibodies to histones were found to be most commonly responsible for the positive antinuclear antibody (ANA) test in asymptomatic patients treated with procainamide, in old people, in patients with neoplastic diseases, and in young women affected with a rheumatoid-like disease. Only in a very few patients were antibodies to dDNA and nucleoproteins demonstrated. Antibodies to nDNA were not found. The antibodies to histones were demonstrated by two methods: absorption of ANA-positive sera with a histone solution and subsequent performance of an ANA test; and acid elution of histones from thyroid sections followed by histone reconstitution.

Adolescent↗
PubMed1984

Autoallergic reactions induced by procainamide.

Procainamide has a high propensity for the induction of an autoimmune response. The immune response is highly selective and the autoantibodies so induced are directed against nuclear histones. Acetylator phenotypes play an important role in the immune response, with slow acetylators developing antihistone antibodies much sooner than fast acetylators. In the early detection of drug-induced lupus syndromes, the finding of antihistone antibodies in the absence of other types of antinuclear antibodies greatly aids in establishing the diagnosis.

Acetylation↗
PubMed1993

Epitope mapping of histone 5 (H5) with systemic lupus erythematosus, procainamide-induced lupus and hydralazine-induced lupus sera.

To define the linear epitopes on H5 that react with systemic lupus erythematosus (SLE) and drug-induced lupus (DIL) sera, concurrent overlapping hexameric peptides corresponding to the sequence of H5 were synthesized by stepwise elongation of the polypeptide chains on polyethylene supports. The hexapeptides were tested for reactivity with 8 SLE and 8 DIL sera using an enzyme linked immunosorbent assay (ELISA). SLE and hydralazine-induced lupus (HIL) antibodies were most reactive with peptide 45 (SSRQSI) and patients with procainamide-induced lupus (PIL) were most reactive with peptide 24 (SHPTYS). The epitopes of highest reactivity were in the globular domain of H5. Low reactivity was observed with carboxyl terminal peptides. These findings differ from immunoblotting studies of protease cleaved peptides which have previously shown that the H5 determinants are in the carboxyl terminus.

Amino Acid Sequence↗
PubMed1983

Myocarditis resolving after discontinuation of procainamide.

A patient with dilated cardiomyopathy was proven to have unsuspected severe myocarditis on endomyocardial biopsy. There was no history of an antecedent viral infection. Procainamide therapy had recently been initiated and was discontinued after the biopsy results were available. A repeat endomyocardial biopsy showed resolution of the inflammation.

Aged↗
PubMed1992

Popliteal lymph node enlargement induced by procainamide.

The ability of procainamide (PA) to induce primary local popliteal lymph node (PLN) reactions has been investigated. We employed an in vitro drug-metabolizing system, based on the hypothesis that the negative result for PA in a PLN assay (PLNA) was due to insufficient metabolizing activity at the reaction site. PA was incubated previously in vitro with the S-9 mixture derived from rat liver. The reactants were ultrafiltered in order to eliminate high molecular-weight molecules, and then the low molecular-weight fraction was subcutaneously (s.c.) injected into the hind footpad of mice. PLN reactions were assessed by weighing the popliteal lymph node of the injected side. The reactants of more than 5 mg of PA and S-9 mixture induced PLN enlargement in C3H/He mice 8 days after injection. BALB/c and C57BL/6 mice were also susceptible to PLN reaction in response to the reactants of PA (10 mg) and S-9 mixture. PLN reactions to PA were induced 2 days after the injection and sustained until 18 days. Contact of PA with the S-9 mixture for 30 min at 37 degrees C was sufficient to induce PLN enlargement. However, contact for 24 h reduced the peak reaction. On the other hand, PA which had not been incubated with the S-9 mixture and acetylprocainamide (acetylPA) gave little or no reaction. Local PNA has not been considered to be suitable for the detection of drugs with the potential to induce immune disorders in cases where a metabolite contributes to the adverse reaction. However, the employment of an in vitro drug-metabolizing system may overcome that defect.

Animals↗
PubMed1993

Study of procainamide hapten-specific antibodies in rabbits and humans.

Procainamide (PA) is the drug most commonly associated with the induction of autoantibodies and drug-related lupus (DRL). While the majority of these patients express autoantibodies, antibodies to the parent drug and metabolites, PA-hydroxylamine (PAHA) or nitroso-PA (NOPA), have not been reported in humans. Hapten-carrier conjugates were prepared using human hemoglobin (HgB) or autologous rabbit erythrocytes with PAHA or NOPA. PA was conjugated to rabbit serum albumin (RSA) or egg albumin (OVA) via diazotization and condensation methods. Rabbits were immunized with hapten conjugates in Freund's adjuvant. These hapten-carrier compounds (5-10 micrograms/ml) were used as test antigens for antibodies in sera from the rabbits and 40 patients on chronic PA treatment. 10 SLE patients, 33 elderly and 20 young normal controls by ELISA. Type I and II collagens were also used as test antigens for human sera. Sera from rabbits immunized with the PA compounds had elevated IgG antibody values to PA, PAHA and NOPA, but no autoantibodies. Absorption of the rabbit sera with the PA compounds reduced the antibody levels; ssDNA and histones failed to inhibit the total binding values. Mean binding to PA-OVA was 0.95 +/- 0.41 for PA patients and 1.37 +/- 0.26 standard error of means (S.E.M.) in the SLE patients compared to 0.37 +/- 0.14 S.E.M. in the normal sera (P < or = 0.05); similar binding values to PAHA-HgB and NOPA-HgB were also observed. Sixty-eight percent of the PA patients had antibodies to type II collagen. Elevated binding values to PA compounds were inhibited by absorption of human sera with ssDNA or total histones; absorption with PA or PAHA had no significant effect. These findings suggest that sera from PA patients containing high titers of autoantibodies cross-react in vitro with unrelated antigens.

Adult↗
PubMed1991

Use of 7,7,8,8-tetracyanoquinodimethane for spectrophotometric determination of certain local anaesthetics and procainamide hydrochloride.

A simple and rapid spectrophotometric procedure has been developed for the determination of four local anaesthetics containing a free primary amine moiety and of procainamide hydrochloride as the drug substances and in dosage forms. The method is based on the reaction of the drug with 7,7,8,8-tetracyanoquinodimethane in alkaline solution to produce yellow products. The chromogen was measured at 473 nm. The effects of several variables on colour development were established. Job's plots of absorbance versus molar ratio of drug to reagent indicated a 1:1 ratio for all the drugs studied. Results of the analysis of drug substances and their dosage forms by the proposed method are in good agreement with those obtained by the USP XX method.

4-Aminobenzoic Acid↗
PubMedDate not supplied

Intravenous procainamide for the conversion of new onset atrial fibrillation in the emergency department setting.

A common problem seen by emergency physicians, that of new onset atrial fibrillation, and a unique approach to its emergency department management are discussed. In hemodynamically stable patients with new onset atrial fibrillation, an attempt at chemical cardioversion can be made in the emergency department with intravenous procainamide at a rate of 20 mg/min to a maximum dose of 20 mg/kg if accompanied with careful monitoring of blood pressure and cardiac rhythm. If cardioversion is successful, such individuals may not require hospitalization if they are less than 65 years of age and without evidence of organic heart, lung, or thyroid disease.

Atrial Fibrillation↗
PubMed2005

Effect of 5-azacytidine and procainamide on CD3-zeta chain expression in Jurkat T cells.

It has been observed that decrease of DNA methyltransferase 1 (DNMT1) activity is associated with low content of the CD3-zeta (zeta) chain in T cell receptor (TCR)/CD3 complex of T cells in systemic lupus erythematosus (SLE) patients. The CD3-zeta chain plays a pivotal role in intracellular signal transmission between TCR/CD3 complex and nuclei. The compounds 5'-azacytidine (AZC) and procainamide (PCA) belong to inhibitors of DNMT1, whose low activity correlates with increase in transcription of various genes. Using the reverse-transcription and real-time quantitative PCR (RQ-PCR) analysis, we indicated that AZC and PCA did not profoundly affect on CD3-zeta chain transcription in Jurkat T leukemia cells clone E6-1. However, the flowcytometric analysis revealed that AZC and PCA decreased intracellular contents of CD3-zeta chain in these cells in dose dependent manner. Our results suggest that decrease of DNMT1 activity may alter intracellular signal transmission without effect on transcription level of CD3-zeta chain.

Anti-Arrhythmia Agents↗
PubMed2003

Characterisation of recombinant HERG K+ channel blockade by the Class Ia antiarrhythmic drug procainamide.

Class Ia antiarrhythmic drugs, including procainamide (PROC), are associated with cardiac sodium channel blockade, delayed ventricular repolarisation and with a risk of ventricular pro-arrhythmia. The HERG K(+) channel is frequently linked to drug-induced pro-arrhythmia. Therefore, in this study, interactions between PROC and HERG K(+) channels were investigated, with particular reference to potency and mechanism of drug action. Whole-cell patch-clamp recordings of HERG current (I(HERG)) were made at 37 degrees C from human embryonic kidney (HEK 293) cells stably expressing the HERG channel. Following activating pulses to +20 mV, I(HERG) tails were inhibited by PROC with an IC(50) value of approximately 139 microM. I(HERG) blockade was found to be both time- and voltage-dependent, demonstrating contingency upon HERG channel gating. However, I(HERG) inhibition by PROC was relieved by depolarisation to a highly positive membrane potential (+80 mV) that favoured HERG channel inactivation. These data suggest that PROC inhibits the HERG K(+) channel by a primarily 'open' or 'activated' channel state blocking mechanism and that avidity of drug-binding is decreased by extensive I(HERG) inactivation. The potency of I(HERG) blockade by PROC is much lower than for other Class Ia agents that have been studied previously under analogous conditions (quinidine and disopyramide), although the blocking mechanism appears similar. Thus, differences between the chemical structure of PROC and other Class Ia antiarrhythmic drugs may help provide insight into chemical determinants of blocking potency for agents that bind to open/activated HERG channels.

Anti-Arrhythmia Agents↗
PubMed1981

High performance liquid chromatographic analysis of the antiarrhythmic drugs procainamide, disopyramide, quinidine, propranolol and metabolites from serum extracts.

We describe a method for the simultaneous high performance liquid chromatographic determination of several antiarrhythmic drugs and some of their metabolites after extraction from 2.5 mL of spiked pooled sera. The extracts were applied to a C8 reversed phase column. Nine compounds of interest were resolved within the 30 minute run. An initial mobile phase of 80% phosphate (25 mmol/L, pH 3.5), 20% organic (acteonitrile:methanol, 2:3) was maintained for 2 min at which time a linear gradient was used to change the mobile phase to 30% phosphate, 70% organic at 20 min after injection. This composition was maintained from an additional 5 min. Absorbance at 212 nm was used for detection. Peak area ratios of drug to internal standard (N-propionylprocainamide) were used for quantitation. The relative standard deviations (and mean solute concentrations) of daily duplicate determinations for 15 days are: procainamide, 5.1% (5.9 mg/L); N-acetylprocainamide, 9.3% (6.0 mg/L); Mono-N-dealkyldisopyramide, 3.7% (4.1 mg/L); disopyramide, 4.3% (4.0 mg/L); quinidine, 4.5% (6.5 mg/L); and propranolol, 5.1% (0.097 mg/L). Dihydroquinidine and 4-hydroxypropranolol were also resolved but not quantitated.

Acecainide↗
PubMed1997

Direct determination of procainamide and N-acetylprocainamide by capillary zone electrophoresis in pharmaceutical formulations and urine.

In this work a new sensitive capillary zone electrophoresis method for the direct determination of procainamide (PA) and N-acetylprocainamide (NAPA) in pharmaceutical formulations and urine samples without any extraction and/or preconcentration steps has been developed. The determination was carried out in a fused-silica capillary of 43.5 cm (35.9 cm length to the detector) x 0.75 micron J.D. Phosphate 0.05 M buffer was used as the background electrolyte and 10 kV separation voltage was applied. The separation of PA and NAPA is possible in a wide range of pH from 1.7 to 9.7. However, in order to avoid the effect of the urine matrix, it is optimal to work at pH 7.7. The determination of PA and NAPA takes less than 5 min while high resolution is achieved. The detection limits obtained, 1.235 micrograms/ml and 0.359 microgram/ml for PA and NAPA respectively, are lower than those for GC method normally reported.

Acecainide↗
PubMed1984

Antifibrillatory drugs: the case for lidocaine and procainamide.

Ventricular fibrillation (VF), in most instances, is sustained by multiple wavefronts. The most important prerequisites for development and maintenance of VF are inhomogeneity in activation and recovery and shortening of refractoriness. If drugs are to be effective in removing VF or facilitating its electrical removal, this should occur by alteration of these electrophysiologic mechanisms. Assessment of the antifibrillatory properties of many drugs has been compromised by at least two factors: 1) the questionable appropriateness of the model, and 2) the failure to distinguish between prevention of VF and removal, or facilitation of electrical removal, of VF. Most instances of VF encountered clinically are secondary to acute ischemia; therefore, the most applicable model is acute myocardial ischemia with spontaneous VF. In this setting little is known about the effectiveness of lidocaine (L) or procainamide (PA). While there is more information regarding the role of L in prevention of VF, and of both L and PA in elevating ventricular fibrillation threshold, there is a lack of data on the roles of either drug in removal of existing VF. Thus we are left to speculate on the actions of L and PA that may account for their usefulness in the treatment of VF. These actions are the basis for a projection of the role of L and PA in the treatment of VF. There is evidence in animal models of acute myocardial ischemia to support the use of at least lidocaine in VF.

Electrophysiology↗
PubMed1998

Genetic and immunologic studies of patients on procainamide.

Forty (40) patients with cardiac arrhythmias receiving procainamide (PA) therapy and 24 patients who were receiving other drugs for their cardiac disorders were investigated for class II HLA phenotypes and their DRB1*04 and DQB1*03 subtypes. Other genetic marker evaluations in the PA patients included: 1) class III MHC C4A and C4B null alleles of complement; and, 2) acetylation phenotype. Twenty (20) of the PA patients were also tested for the ability of their stimulated cells to secrete Interleukin-1 (IL-1 beta) and tumor necrosis factor (TNF alpha). We also examined the spontaneous production of these cytokines by peripheral blood leukocytes (PBL) from patients who were receiving chronic PA treatment. The results revealed no association of acetylation phenotypes with the class II HLA phenotypes nor class III MHC C4 allotypes in these patients. The results did show a significant increase in class III C4 complement allotypes in the PA patients when compared to the controls. The results also showed a significant increase in autoantibodies and DQw3 phenotypes in the PA patient group when compared to control populations. Results of spontaneous IL-1 and TNF production suggested there may be an association of select class II HLA phenotypes in some patients and this may be relevant to host responsiveness to PA treatment.

Acetylation↗