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PubMed1988

Dose dependent effect of cimetidine on procainamide disposition in man.

This study investigated the influence of single dose of 200 mg and 400 mg cimetidine on the pharmacokinetics of procainamide (PA) in healthy Chinese. The results show that AUC of PA was significantly raised by 38% and 24% with a significant reduction in renal clearance by 40% and 31%, respectively, when single dose of 400 mg or 200 mg cimetidine was coadministered. Significant changes of AUC and renal clearance of the active metabolite--N-acetylprocainamide (NAPA) were found only following the dose of 400 mg cimetidine. The larger dose of cimetidine produced greater alteration in the PA and NAPA pharmacokinetics. The interaction is mainly associated with their reduced renal clearance.

Acecainide↗
PubMed1989

[Ion pair HPLC determination of p-aminobenzoic acid as an impurity in procaine and procainamide hydrochlorides].

A simple, specific and sensitive high-performance liquid chromatographic method for the determination of p-amino benzoic acid (PABA) as impurity in procaine and procainamide hydrochlorides has been developed. The compounds were chromatographed on reversed phase C-18 using water-methanol-acetonitrile solvent system containing sodium lauryl sulphate ion-pair reagent.

4-Aminobenzoic Acid↗
PubMed1988

Procainamide-induced urticarial vasculitis.

Dermatologists are often faced with the difficulty of evaluating drug reactions in patients receiving multiple medications. Unfortunately, few drugs produce distinctive lesions; many types of medications can produce identical eruptions. One common drug-induced eruption is urticaria. We report a specific eruption due to procainamide: urticarial vasculitis.

Aged↗
PubMed1988

Pure red cell aplasia in procainamide induced systemic lupus erythematosus. Report and review of the literature.

We describe a patient who developed pure red cell aplasia as part of a lupus-like syndrome while taking procainamide. Pure red cell aplasia resolved spontaneously after discontinuation of this drug. Although pure red cell aplasia has been reported in several patients with idiopathic systemic lupus erythematosus (SLE), this represents the first such report in a patient with drug induced SLE.

Aged↗
PubMed1988

Hydralazine and procainamide inhibit T cell DNA methylation and induce autoreactivity.

Inhibitors of DNA methylation, such as 5-azacytidine, induce gene expression. We have previously reported that cloned T cells treated with 5-azacytidine lose the requirement for Ag and can be activated by autologous HLA-D molecules alone, thus becoming auto-reactive. This phenomenon could potentially mediate an autoimmune disease in vivo. Inasmuch as several drugs are known to cause autoimmune disease, we asked whether they exert the same effects on T cells as 5-azacytidine. We report that hydralazine and procainamide, two drugs associated with a lupus-like autoimmune disease, also inhibit DNA methylation and induce self-reactivity in cloned T cell lines. These results suggest that drug-induced autoimmune disease may be due to activation of as yet unidentified genes through mechanisms involving DNA methylation.

Autoimmune Diseases↗
PubMed1987

Cytotoxicity of oxidative metabolites of procainamide.

Indirect evidence suggests that metabolism of procainamide (PA) may be necessary for generation of its autoimmunity-inducing capacity. Reactive metabolites of PA produced by hepatic mixed function oxidases have been identified by their capacity to bind proteins covalently. The present study extends these findings by comparing the toxicity of various chemically synthesized metabolites of PA to a variety of cell lines and primary cultures. PA and its N-acetyl- and N-acetyl-N-oxide-derivatives were nontoxic to S49.1 cells at concentrations up to 5 mM, whereas nitro-Pa (4-nitro-N-(diethylaminoethyl)benzamide hydrochloride) and azoxy-PA (bis-N,N'-(diethylaminoethyl)-4,4'-azoxydibenzamide) displayed partial cytotoxicity at 1 and 0.1 mM, respectively. (The therapeutic range of PA is 0.02-0.05 mM.). In contrast, hydroxylamine-PA (4-hydroxylamino-N-(diethylaminoethyl)benzamide hydrochloride) was highly cytotoxic, producing a TD50 between 0.002 and 0.045 mM among the eight cell lines tested. Hydroxylamine-PA sensitivity correlated with cell reducing capacity, suggesting that redox cycling contributes to cytotoxicity. The hydroxylamine metabolite of PA undergoes spontaneous air oxidation to the nitroso-derivative (nitroso-PA). When this oxidation was minimized by rapid manipulations or inhibited by ascorbic acid, cytotoxicity was reduced or eliminated, suggesting that the nitroso-derivative may be the toxic metabolite. Quiescent peripheral blood lymphocytes, especially T-cells, were relatively insensitive to hydroxylamine-PA when evaluated by dye exclusion 1 day after drug exposure. However, massive DNA strand breaks were detectable in these cells immediately after drug exposure, and resting lymphocytes treated with 0.01 mM hydroxylamine-PA died slowly during the subsequent week.(ABSTRACT TRUNCATED AT 250 WORDS)

Ascorbic Acid↗
PubMed1987

Comparable steady-state bioavailability between two preparations of conventional-release procainamide hydrochloride.

The pharmacy and therapeutics committee-based clinical evaluation can be a useful tool in the economic and functional effectiveness of a restrictive formulary system. We utilized this concept to evaluate a generic formulation of procainamide hydrochloride (PA) for admission to our formularies. The study performed was a randomized, single-blind, crossover comparison of the serum-concentration profiles of two preparations (Squibb vs. Ascot) of conventional-release PA. Ten outpatients requiring chronic PA therapy for the control of ventricular dysrhythmias were evaluated. The resultant dose-adjusted data showed no significant difference between mean serum PA concentrations at any sample time, area under the serum concentration-time curves, mean peak serum PA concentrations achieved, or peak-trough fluctuations. Relative bioavailability was calculated to be 0.972 +/- 0.59. The Ascot preparation demonstrated a delay of 15 minutes before the onset of absorption; however, it also showed an earlier tmax in comparison to the Squibb formulation. Generic substitution of Ascot PA in place of Squibb PA may be implemented with significant cost savings.

Aged↗
PubMed1979

Nephrotic syndrome in procainamide induced lupus nephritis.

We report a case of the nephrotic syndrome occurring in a patient with procainamide induced LE. It was associated with bilateral pleural effusions, pericarditis, fever, positive LE cell preparation and a high titer of antinuclear antibodies. No anti-DNA antibodies were found. Renal biopsy showed mesangial proliferation with few IgM and C3 deposits and interstitial infiltrates; electron microscopy revealed subendothelial deposits. Clinical improvement occured after steroid therapy and there was no recurrence 24 months after withdrawal of prednisone.

Aged↗
PubMed1974

Procainamide-induced SLE and lymphoreticular disorders.

A 56-year-old male patient diagnosed as a case of procainamide-induced systemic lupus erythematosus (SLE) was found to have a lymphoproliferative disorder at postmortem examination.Contrary to other immune disorders, the association of SLE with neoplasia is a rare occurrence. The present case raises the question of whether a relationship exists between the lupus diathesis and lymphoreticular neoplasia. The study of the incidence of neoplasia in families of patients with SLE may prove helpful in establishing this relationship.

Aortic Diseases↗
PubMedDate not supplied

Procainamide-induced lupus erythematosus: report of a case with a large pericardial effusion and fluid analysis.

A patient with procainamide lupus erythematosus had a large pericardial effusion. As in other reported cases histology revealed a fibrinous mononuclear pericarditis and the pericardial fluid was a serosanguinous inflammatory exudate with a high LDH level and normal glucose concentration. The ANF and LE cell preparation were positive in the fluid but the C3 complement was normal. The frequency of pericarditis is similar in systemic and drug-induced lupus erythematosus yet low complement levels need not occur. Complement activation may therefore be unnecessary for the development of either type of lupus pericarditis.

Complement System Proteins↗
PubMed1977

Effects of procainamide and chloramphenicol on acute vasospasm.

The basilar artery of the dog was exposed through the clivus and made spastic by puncture or by topical application of 5% barium chloride. Injections of procainamide or chloramphenicol into the vertebral artery or into a peripheral vein had no discernable effect on the acute vasospasm. Topical application of 0.1% to 10% concentrations of either of these drugs effected definite vasodilation, with the extent and rapidity of vasodilation increasing with increasing concentrations. Lesser concentrations were ineffective.

Acute Disease↗
PubMed1980

Comparison of the autonomic effects of procainamide and N-acetylprocainamide in the dog.

The autonomic effects of procainamide (PA) and N-acetylprocainamide (NAPA) were studied in anesthetized dogs. High plasma concentrations of PA (31 +/- 1.3--64 +/- 3.4 micrograms/ml) and NAPA (64 +/- 3.4--127 +/- 8.3 micrograms/ml)) reduced base-line mean arterial pressure and heart rate and attenuated the pressor and positive chronotropic responses to bilateral carotid occlusion and the negative chronotropic response to vagal stimulation. Neither drug reduced the pressor or positive chronotropic responses to catecholamines (epinephrine, phenylphrine, isoproterenol), however. In fact, at some doses PA and NAPA accentuated the pressor and positive chronotropic effects of epinephrine. Similarly, the depressor response to acetylcholine was not reduced by these drugs; it was significantly increased at some doses. In the isolated hindlimb (constant flow) PA and NAPA reduced the pressor response to preganglionic (sympathetic chain) stimulation but not to postganglionic (femoral and sciatic nerves) stimulation. We conclude that NAPA, like PA, at high plasma levels is vagolytic and attenuates baroreceptor-mediated reflexes associated with reduced arterial pressure. These effects appear to be due to ganglionic blockade.

Acecainide↗
PubMed1981

In vivo and in vitro antiarrhythmic and arrhythmogenic effects of N-acetyl procainamide.

We studied the effects of N-acetyl procainamide (NAPA) on isolated canine cardiac tissues by using standard microelectrode techniques. NAPA (10-40 mg/l) does not suppress the rate of phase 4 depolarization of Purkinje fibers and does not change resting membrane potential, action potential amplitude or maximum upstroke velocity of phase O of the action potentials of Purkinje fibers or ventricular muscle cells. In contrast, action potential duration of both types of cells is significantly prolonged by NAPA in a dose-dependent manner. In toxic concentrations (80-240 mg/l), NAPA can produce a "secondary plateau" at about -55 mV during phase 3 of the action potential of Purkinje fibers driven at cycle lengths of 2000 to 4000 msec. Early afterdepolarizations and single or multiple spontaneous action potentials were often triggered during the secondary plateau. When NAPA is given to conscious or anesthetized dogs (50-100 mg/kg i.v.), ventricular extrasystoles occur at constant coupling intervals if the basic rate of ventricular activation is slow (60 per minute or slower). Single extrasystoles, or the first extrasystole in a salvo, appear at coupling intervals of 400 to 600 msec. The single and multiple extrasystoles induced by NAPA may be caused by action potentials triggered during the secondary plateau and may degenerate into ventricular fibrillation. In doses of up to 100 mg/kg i.v., NAPA exerts slight antiarrhythmic effects in dogs with 24-hr myocardial infarcts.

Acecainide↗
PubMed1981

[Dynamic electrocardiography evaluation of the effectiveness of prajmalium bitartrate, disopyramide and procainamide in patients with stabilized ventricular extrasystole].

20 patients with chronic premature ventricular contractions (P.V.Cs) underwent several Holter ECG monitorings to assess clinical effectiveness of three antiarrhythmic drugs: Prajmalium Bitartrate (P.B.) 80 mg/daily, Disopyramide (D.) 600 mg/daily and Procainamide (P.) 2400 mg/daily, to assess the most effective antiarrhythmic medication in every patient. Clinical effectiveness was considered as 80% reduction of P.V.Cs or 50% reduction with suppression of all complex ventricular ectopy (repetitive, polymorph, bigeminy). These results were observed respectively, for 80% reduction, in 5/20 patients for P.B., in 9/20 for D., and in 3/19 for P; and for 50% reduction in 11/20 for P.B., in 18/20 for D., and in 9/19 for P. Comparison in the same patient, using Holter ECG monitoring with a computer assisted analysis, of the effects of different antiarrhythmic medications, is a rational procedure to assess clinical efficacy of new antiarrhythmic drugs and to choose the most effective in each case.

Adolescent↗
PubMed1982

Theophylline, dyphylline, caffeine, acetaminophen, salicylate, acetylsalicylate, procainamide, and N-acetylprocainamide determined in serum with a single liquid-chromatographic assay.

We describe a single set of liquid-chromatographic conditions for assay of theophylline, dyphylline, caffeine, acetaminophen, salicylate, acetylsalicylate, procainamide, and N-acetylprocainamide in serum. The chromatographic system includes a Waters Associates mu-Bondapak C18 column and acetonitrile in 0.1 mol/L potassium phosphate buffer, pH 4.0 (9.75/90.25 by vol), as the mobile phase. Only 50 microL of serum is required, and drug concentrations as low as 0.5 mg/L can be detected. Absolute and relative analytical recoveries range from 95 to 101%. Day-to-day variation of the method is less than 6% for each drug. Linearity extends to 1 g/L for all drugs. Recycling of the mobile phase under pressure eliminates the need to prepare and de-gas solvents. The use of the single stationary and mobile phase provides a practical and economical approach to routine and urgent therapeutic drug monitoring.

Acecainide↗
PubMed1978

The quantitative disposition of procainamide and N-acetylprocainamide in the rat.

The objectives of this study were to investigate: 1) the rat acetylator phenotype, 2) the systemic availability of oral procainamide (PA), 3) the kinetic disposition of PA and its N-acetyl metabolite (NAPA) and 4) the relationship between PA dose and steady-state blood PA and NAPA levels. The rat acetylator phenotype seems to be monomorphic in type. The systemic availability of PA was estimated to be 78%. The half-life (T 1/2) of PA elimination was 55 minutes and that of NAPA was 51 minutes. PA clearance was 64 ml/kg/min and NAPA clearance 22.4 ml/kg/min. The apparent distribution volume for PA was 4.92 liters/kg and for NAPA 1.64 liters/kg. Acetylation accounted for 38% of PA disposition, urinary excretion 34% and other metabolism 28%. Urinary excretion of NAPA accounted for 72% of administered drug. Steady-state blood PA levels showed a linear increase with dose whereas NAPA did not. The latter observation suggests saturation of PA acetylation at higher PA doses.

Acetylation↗
PubMed1978

Capacity-limited elimination of procainamide in man.

Procainamide (PA) pharmacokinetics were studied at steady state in 19 patients. The PA was given as 1.0 or 1.5 g eight hourly (L and H dose groups) and acetylator phenotype determined from sulphadimidine acetylation was classified as Slow or Fast (S or F). Thus, four groups were categorized, HF, LF, HS and LS with 7, 5, 3, and 4 patients in each respective group. Overall the mean steady state plasma concentration of PA (Cpss) expressed as a fraction of dose did not depend on dose or on acetylator status, but the HS group had significantly higher Cpss per gram dose (6.3 mug/ml) than LS (2.7 mug/ml) or the HF (2.3 mug/ml) groups. Clearance of PA be acetylation (C1A) was 23.8% of the total in fast acetylators and 16.5% in slow acetylators. C1A was not dose-dependent in the HF or LF groups (mean 177.9 ml/min and 168.4 ml/min) but was dose-dependent in the HS group (mean 74.6 ml/min) which differed significantly from the LS group (mean 113.4 ml/min).

Acetylation↗
PubMed1981

Liquid-chromatographic determination of antidysrhythmic drugs: procainamide, lidocaine, quinidine, disopyramide, and propranolol.

We present a method for the analysis of antidysrhythmic drugs [procainamide, acecainide (NAPA), lidocaine, quinidine, disopyramide, N-desisopropyl disopyramide, and propranolol] in serum. The drugs, together with an internal standard, are extracted from 0.2-1.0 ml of serum, separated on an octyl-bonded reversed-phase column using a mobile phase consisting of acetonitrile/phosphate buffer, and monitored by either ultraviolet or fluorescence spectrophotometry. The proposed method offers good reproducibility, sensitivity, linearity, and accuracy. Of more than 50 drugs and metabolites, tested for possible interference, only diazepam, flurazepam, and the N-oxide metabolite of quinidine interfere with quinidine analysis, while meperidine coelutes with disopyramide. However, diazepam and flurazepam do not interfere with quinidine analysis with fluorescence detection.

Anti-Arrhythmia Agents↗