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PubMed1987

[Comparison of the effects of ajmaline and procainamide in the diagnosis of paroxysmal atrioventricular block].

14 suspected of having a paroxystic atrio-ventricular block underwent a complete electrophysiological exploration including an ajmaline test. It was administered at the standard dose of 1 mg/kg at the rate of 1 mg/s. In order to evaluate a replacement test, an equivalent dose of procainamide was injected at the same rate (10 mg/kg, 10 mg/s) a few hours later. In 4 out of 14 cases the ajmaline test was positive. In only one patient, procainamide was able to demonstrate a sub-nodal block. The maximal lengthening of HV occurred at an earlier time after ajmaline than after procainamide (2.2 +/- 0.75 min. versus 4.1 +/- 1.59 min, p less than 0.02) and certainly more clear-cut (MaxHV = 73.5 +/- 12.9 ms versus 59.5 +/- 12.1 ms, p less than 0.01). The lengthening of HV after administration of these two products was significantly correlated but always markedly lesser with procainamide. In conclusion, the procainamide is less sensitive than the ajmaline test in the positive diagnosis of paroxystic atrio-ventricular blocks concerning absolute criteria in the positive diagnosis as well as relative criteria such as a definite lengthening of HV with ajmaline.

Aged↗

PubMedDate not supplied

Predicting plasma procainamide concentrations resulting from a sustained-release preparation.

Two methods of predicting plasma procainamide concentrations (PPCs) for a sustained-release procainamide (SRP) dosage form were compared using previously published data on 12 healthy subjects. Methods A and B were both based on a one-compartment pharmacokinetic model requiring an elimination rate constant and area under the concentration-time curve from an immediate-release oral procainamide dosage form and in vitro dissolution data from the SRP product. Method A also used an absorption rate constant. The predicted versus measured PPCs for two sets of peak and trough concentrations in each subject were evaluated using linear regression. The mean predicted PPCs by both methods followed the measured PPCs closely; however, the time of peak concentration was predicted more accurately by method A. The evaluation of predictive performance showed good precision and a small but statistically significant bias with either method, peak values were overpredicted and trough values were underpredicted. These two methods adequately predicted plasma procainamide concentrations in healthy subjects following a sustained-release procainamide preparation.

Delayed-Action Preparations↗

PubMedDate not supplied

Metabolism of procainamide to a hydroxylamine by rat and human hepatic microsomes.

We have previously demonstrated that procainamide is oxidized to a reactive metabolite. We speculated that this reactive metabolite might be a hydroxylamine and further that it might be responsible for the syndrome of procainamide-induced lupus. We now report that procainamide is metabolized to a hydroxylamine by rat and human hepatic microsomes. The extent of this metabolic oxidation was quantitated by HPLC after conversion of the hydroxylamine to the more stable nitro derivative of procainamide. Formation of the hydroxylamine required NADPH, active microsomes, and oxygen and was inhibited by carbon monoxide, SKF 525-A, and cimetidine. Formation of the hydroxylamine was also studied as a function of time, microsomal protein concentration, and procainamide concentration.

Adult↗

PubMed1982

Excretion of procainamide into bile and saliva in rats with chronic renal failure.

The excretion of the widely used antiarrhythmic agent procainamide into the bile and saliva of rats with chronic renal failure (CRF) induced by a two stage-total nephrectomy was studied. Chronic renal failure significantly elevates plasma, salivary, and biliary procainamide levels compared to normal and sham operated rats at all time periods studied. However, while the increase in salivary excretion parallels that of plasma, biliary excretion does not. Results indicate that there is probably saturation of an active transport mechanism for procainamide into bile and that bile cannot compensate for increased drug levels which accumulate during CRF. Salivary excretion, though increased during CRF, also cannot compensate for elevated procainamide levels. Moreover, CRF does not appear to impair non-microsomal acetylation of procainamide, the major biotransformation reaction in the metabolism of this drug.

Acecainide↗

PubMed1983

Inhibition of ouabain-induced increase in Na content of cultured myocardial cells by quinidine and procainamide.

Addition of ouabain caused gradual increases of both the Na content of cultured myocardial cells and the rate of Ca++ uptake by the cells. Ouabain-induced irregular beating of the cells (ouabain toxicity) appeared to develop when the Na content and the rate of Ca++ uptake exceeded about 1.5 and 2.0 times, respectively, the normal levels. Quinidine and procainamide prevented ouabain-induced increases of the Na content and the rate of Ca++ uptake as well as ouabain-induced toxicity. The problem of how quinidine and procainamide counteract the effects of ouabain was then studied. Quinidine and procainamide did not affect the Na+-Ca++ exchange activity. Na+,K+-adenosine triphosphatase activity, Na+-pumping out activity or ouabain-binding activity of myocardial cells, but inhibited passive Na+ influx, which is achieved by a simple diffusion system. From these observations, it is suggested that inhibition by quinidine or procainamide of passive Na+ influx indirectly prevents ouabain-induced increase in the intracellular Na content of myocardial cells and that this presumably explains at least in part the inhibitory effect of quinidine and procainamide on ouabain-induced irregular beating.

Animals↗

PubMed1983

Procainamide uptake by rabbit proximal tubules.

Procainamide is an organic cation and commonly prescribed drug that is actively secreted into the urine by renal proximal tubules. In order to elucidate further the mechanisms involved in this secretion, [3H]procainamide uptake into dissected S2 segments of superficial proximal tubule cells was studied. Uptake of [3H]procainamide was reduced by hypothermia and in a dose-related manner by the organic cations nonradiolabeled procainamide, cimetidine and quinidine and also by the carbonic anhydrase inhibitors acetazolamide and benzolamide, but not by ouabain. All these drugs were shown previously to inhibit transtubular secretion of [3H]procainamide in isolated perfused proximal tubules. The results of these and our previous studies suggest that 1) organic cations reduce the tubular secretion of each other, in part, by competing for uptake across the basolateral membrane of renal tubule cells, 2) acetazolamide and benzolamide reduce urinary excretion of organic cations, in part, by inhibiting proximal tubular secretion and 3) the potential difference across the basolateral cell membrane (due to activity of Na+-K+-dependent adenosine triphosphatase) is not the only driving force for uptake of organic cations into intact renal tubule cells.

Animals↗

PubMed1982

Contrasting effects of verapamil and procainamide on intraventricular conduction and reentry within the His-Purkinje system in man.

The effects of intravenous verapamil (0.15 mg/kg) and procainamide (12-14 mg/kg) on intraventricular conduction and reentry within the His-Purkinje system were studied in eighteen patients using His bundle electrograms and ventricular extrastimulus method. Verapamil's effects were studied in eight patients and procainamide's effects in ten patients. Plasma verapamil concentrations ranged from 56 to 192 ng/ml (mean +/- SD: 139.0 +/- 46.0); plasma procainamide concentrations ranged from 11.3 to 19.0 mg/liter (mean +/- SD: 14.9 +/- 2.5). Verapamil caused no change in latency, intramyocardial conduction (duration of QRS complex), and His-Purkinje (V2H2 interval) conduction of even the earliest premature impulses introduced before the completion of repolarization of the His-Purkinje system and the ventricular myocardium, i.e. when some fibers were presumably at the level of membrane potential at which conduction becomes, wholly or in part, dependent on slow inward calcium current. Verapamil did not abolish or modify the zone of reentry, and did not significantly change the determinants of reentry in any of the eight patients. In contrast, procainamide significantly prolonged the latency, the duration of QRS complex and the V2H2 interval in each of the ten patients, abolished reentry in seven patients, and decreased the width of reentry zone in three patients. The contrasting effects of verapamil and procainamide on intraventricular conduction and reentry within the His-Purkinje system suggest that slow conduction of early premature impulses is due to an incompletely reactivated rapid inward sodium current and not to a fully activated slow inward calcium current. Further, our observations suggest that the system responsible for slow conduction cannot be recognized from the magnitude of conduction delay.

Adult↗

PubMedDate not supplied

Procainamide: a perspective on its value and danger.

Procainamide remains one of the most widely used antiarrhythmic agents in clinical practice. Currently, it is widely used alone or in combination with class I agents (eg, mexiletine or tocainide) to prevent recurrent ventricular tachycardia or symptomatic nonsustained ventricular tachycardia. Procainamide is also used for short-term treatment of ventricular tachycardia and a variety of supraventricular tachycardias, primarily atrial flutter and atrial fibrillation. Long-term procainamide therapy is limited by a number of systemic side effects, primarily lupus-like syndrome, gastrointestinal disturbances, and autoimmune blood dyscrasias. Procainamide levels can be useful in initial dose titrations; however, QRS and QT interval measurements help prevent drug toxicity. It is recommended that patients being started on antiarrhythmic therapy with procainamide be admitted to the hospital for monitoring to ensure that their QT interval is not excessively prolonged.

Anti-Arrhythmia Agents↗

PubMed1998

The influence of moderate and chronic exercise training on the pharmacokinetics of procainamide and N-acetylprocainamide.

The effect of moderate and prolonged exercise on the disposition and metabolism of drugs has not been extensively examined. The present study examined the effect of exercise training on the pharmacokinetics of procainamide and its active metabolite, N-acetylprocainamide. Male Sprague Dawley rats were randomly assigned to three testing groups: (1) sedentary, (2) 4 weeks of exercise training and (3) 8 weeks of exercise training. Treadmill speed and exercise duration were gradually increased, reaching a final rate of 24 m min-1 for an hour by the end of the 4-week or 8-week period. Sedentary and exercise trained rats received a single i.p. dose of procainamide (100 mg kg-1). Serial blood samples were collected over a 10 h period and plasma samples were analysed by an UV-HPLC method. Noncompartmental analysis was performed to estimate the pharmacokinetic parameters. The t1/2 of procainamide was significantly (p < 0.05) higher in the 8 week exercise group (331 min) as compared to the sedentary group (77 min). In addition, there was a significant reduction in the amount of N-acetylprocainamide formed after 8 weeks of exercise (AUCNAPA = 739 ng mL-1 min-1). Results of this study suggest that prolonged exercise (8 weeks of training) alters the pharmacokinetics of procainamide by modifying the amount of active metabolite formed.

Acecainide↗

PubMed1984

Procainamide-induced thrombocytopenia.

An 81-year-old female developed marked thrombocytopenia associated with numerous megakaryocytes in the bone marrow, but without anemia or leukopenia, after taking procainamide (3 g/day) for a period of 2 months. Despite continuation of this medication, treatment with prednisone led to rapid rise in platelet count, and withdrawal of steroid was followed by prompt recurrence of thrombocytopenia. The platelet counts returned to normal after discontinuation of procainamide, and readministration of this drug was followed by reappearance of thrombocytopenia. These observations indicate that exposure to procainamide can cause isolated thrombocytopenia, probably due to immune-mediated destruction of platelets, and that treatment with prednisone may be promptly beneficial in patients with procainamide-induced severe thrombocytopenia and bleeding.

Aged↗

PubMed1977

Polyradiculoneuropathy accompanying procainamide-induced lupus erythematosus: evidence for drug-induced enhanced sensitization to peripheral nerve myelin.

Factors involved in the development of an insidious polyradiculoneuropathy in association with a procainamide-induced, lupuslike syndrome were explored. A 73-year-old man with this clinical syndrome had sural nerve changes consisting of loss of large myelinated fibers with evidence of remyelination and Schwann cell proliferation. The patient's lymphocytes showed marked incorporation of tritiated thymidine when cultured with either procainamide or extracts of human peripheral nerve myelin, and there was an enhanced response with the combination. We also found that procainamide-treated rats showed acceleration of lymphocyte sensitization to peripheral nerve myelin as judged by the early development of inhibition of macrophage migration and positive skin tests to extracts of peripheral nerve myelin. These studies suggest that procainamide can enhance lymphocyte sensitization to peripheral nerve myelin and may have predisposed this individual to development of a polyradiculoneuropathy.

Aged↗

PubMed1988

N-acetylprocainamide is a less potent inducer of T cell autoreactivity than procainamide.

We have reported that an inhibitor of DNA methylation, 5-azacytidine, makes cloned, antigen-specific CD4+ T cells autoreactive, and that procainamide and hydralazine mimic this effect. Those results suggested that procainamide and hydralazine may induce autoimmunity by inhibiting DNA methylation and causing T cell autoreactivity. We report now that N-acetylprocainamide, a procainamide derivative that does not induce lupus, is also a DNA methylation inhibitor, but it is 100 times less potent than procainamide in inducing T cell autoreactivity.

Acecainide↗

PubMed1998

Serum procainamide analysis based on acetonitrile stacking by capillary electrophoresis.

Stacking methods are important in capillary electrophoresis (CE) to overcome the poor detection limits. Cationic drugs are difficult to stack because they tend to interact with the capillary wall. As an example of the stacking of the cationic compounds, procainamide, an anti-arrhythmic drug, is analyzed in serum by CE using an acetonitrile treatment. Serum was deproteinized with acetonitrile containing quinine as an internal standard. About 12% of the capillary volume was filled with sample and separated using an electrophoresis buffer composed of triethanolamine, 2-(N-cyclohexylamino)ethanesulfonic acid (CHES) and 20% isopropanol, pH 8.2. Both the triethanolamine and the CHES were critical for the stacking. The addition of isopropanol improved the plate number for the procainamide and decreased the interfering compounds. Procainamide, its metabolite N-acetyl procainamide, and quinine were separated in about 7 min. The CE compared well with an immunoassay method.

Acetonitriles↗

PubMed1987

Comparative efficacy of pirmenol and procainamide in a drug-resistant population with ventricular tachycardia.

The acute antiarrhythmic properties of pirmenol were studied in 12 patients who failed clinical oral drug therapy with a history of a cardiac arrest or sustained ventricular tachycardia (VT). Programmed electrical stimulation studies were performed in ten men and two women with a mean age of 63 +/- 2 years. All patients had inducible ventricular tachycardia by programmed electrical stimulation when they were off all antiarrhythmic therapy. Patients were then tested on procainamide, 1000 mg, administered intravenously, and ventricular tachycardia could be provoked in nine of twelve patients. Pirmenol was given intravenously, 1.1 mg/kg bolus followed by 40 micrograms/kg/min over 40 minutes prior to drug testing. Pirmenol did not significantly change the baseline heart rate, blood pressure, or measured electrocardiographic values from control values. Ten of 12 patients were still inducible to ventricular tachycardia on pirmenol. Procainamide protected one of nine patients against VT induction. In patients still inducible on drug therapy, the VT rate was significantly slowed from 221 beats/min to 166 beats/min on pirmenol and to 200 beats/min on procainamide. The effects of this new antiarrhythmic agent were similar to procainamide in this drug-resistant study population.

Anti-Arrhythmia Agents↗

PubMed1988

Pharmacodynamics of procainamide in patients with ventricular tachyarrhythmias.

The onset and offset of the electropharmacologic effect of procainamide was studied in nine patients with ventricular arrhythmias. Procainamide was given at a constant infusion rate of 0.27 +/- 0.05 mg/kg/min for 50 to 60 minutes to an average total dose of 15.5 +/- 4.4 mg/kg. The QRS interval (used as an index of electropharmacologic effect) at a paced cycle length of 500 ms, and the plasma procainamide concentration were measured simultaneously every 5 minutes during infusion and at frequent intervals for up to 4 hours during a washout period. The average peak plasma concentration was 15.8 +/- 9.6 micrograms/ml and the average maximum QRS interval prolongation was 23.9 +/- 6.8% from baseline. The temporal and static plasma concentration-effect relationships were evaluated by pharmacodynamic modeling and linear regression. For six patients, there was a minimal (less than 2 minutes) delay in the plasma concentration-effect relationship, and the data fit a linear relationship with an average slope of 3.2 +/- 1.1 msec/microgram/ml. For the other three patients, there was a significant delay (3, 10, and 18 minutes respectively) in the plasma concentration-effect relationship. In most patients, the electropharmacologic effect of procainamide is rapid and proportional to plasma concentration; but in a minority of patients, significant delay occurs and could influence the results and interpretation of electropharmacologic studies.

Adult↗

PubMed1975

GLC determination of procainamide in biological fluids.

A GLC method for the determination of procainamide in biological fluids is presented. By using a dipropyl analog of procainamide as an internal standard, both compounds can be chromatographed directly, yielding linear calibration curves and a sensitivity that allows quantitative determination of concentrations as low as 0.1 mug/ml. The extraction procedure was carefully modified to avoid hydrolysis of N-acetylprocainamide, a major metabolite of procainamide. The usefulness of the procedure is demonstrated by following the disappearance of procainamide from the plasma and urine of human subjects treated with the drug.

Chromatography, Gas↗

PubMed1975

pH-dependent secretion of procainamide into saliva.

The relationship between serum and stimulated, mixed saliva concentrations of procainamide was determined in 12 chronically medicated patients. Samples were obtained at times chosen to approximate the maximum and minimum serum concentrations of the drug during a dosing interval. Marked intersubject variability was found in the ratio of saliva to serum concentration of the drug (0.27-8.93). There was no correlation between the dose (milligrams per kilogram per day) and the minimum serum or saliva concentration of procainamide. Saliva pH ranged from 6.3 to 8.0 in eight subjects. The ratio of saliva to serum concentration of procainamide increased with decreasing pH. This result can be largely explained by the pH-dependent ionization and distribution of procainamide, a weak base.

Humans↗

PubMed1978

The pharmacokinetics of slow-release procainamide.

Procainamide was given to 20 patients with normal renal function as an i.v. bolus of 500 mg followed by 1.0 or 1.5 g eight-hourly by mouth in the form of a slow release preparation (Durules). 97.6 +/- 27.1 (SD)% of the oral procainamide was absorbed, the absorption half life being 1.54 h. The elimination half life following the oral formulation was 6.0 +/- 0.8 h, compared to a mean of 3.4 +/- 0.4 h following i.v. administration. Elimination half life following i.v. administration was slightly related to acetylator status, being 2.75 +/- 0.9 h in fast acetylators, and 4.4 +/- 2.4 h in slow acetylators. This dependence on acetylator status was not seen in half life following oral administration. Total body clearance, steady state plasma procainamide and N-acetylprocainamide were not significantly dependent on acetylator status, although a few patients who are slow acetylators had unexpectedly low clearance and high steady state procainamide concentrations when given the higher dose.

Biological Availability↗