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PubMed1988

Pharmacokinetics of procainamide in continuous ambulatory peritoneal dialysis.

Procainamide (PA) and N-acetylprocainamide (NAPA) pharmacokinetics were examined in six patients undergoing continuous ambulatory peritoneal dialysis (CAPD) following a single oral dose of 625 mg of procainamide HCl. Peak serum PA concentrations occurred between 1 and 3 h after drug administration whereas peak NAPA levels were reached 14 to 48 h following the administration of PA. NAPA levels 1.2 mcg/ml or greater were present for 72 h and in four of the six subjects little further decline occurred at 96 h. PA total body clearance (TBC) averaged 143 ml/min; TBC for NAPA was 29.8 ml/min. PA and NAPA half-lives were considerably prolonged averaging 26.0 and 42.8 h, respectively. V beta for PA was 4.1 l/kg and for NAPA was 1.46 l/kg. PA and NAPA dialysance varied from 0.28 to 5.55 ml/min and from 1.74 to 7.20 ml/min, respectively. This, in turn, represented less than 5 and 25% of the TBC for each drug.

Acecainide↗
PubMed1989

Procainamide-induced circulating anticoagulants in a congenitally-deficient factor XI patient.

A 70 year old male patient admitted for coronary bypass surgery presented with a procainamide-induced lupus syndrome. This syndrome included a LLAC with a positive IgM ACA titer as well as a factor XII inhibitor. These drug-induced inhibitors were superimposed upon the patient's congenital deficiency of factor XI. The methods used to identify these abnormalities are described together with the replacement therapy employed to cover the surgical procedure. The long-term withdrawal of procainamide was associated with correction of all coagulation abnormalities except the factor XI deficiency.

Aged↗
PubMed1989

[New anti-arrhythmia drug. III. Comparative studies of the effects of N-propionylprocainamide, procainamide and N-acetylprocainamide on hemodynamics and cardiac blood flow].

Procainamide (PA) often applied in cases of ventricular arrhythmias causes numerous cardiac and extracardiac undesirable symptoms. Its active metabolite, N-acetylprocainamide (NAPA; Acecainide) is known to affect less noxiously the ventriculo-atrial conduction and the intraventricular++ conduction, and it does not impair contractility of the heart muscle. Many drugs with proven antiarrhythmic activity cannot be used in clinical practice because of disadvantageous effects on the function of the left ventricle and on the coronary blood flow, particularly in patients with the recent myocardial infraction. It seems that another acyl derivative of procainamide with potential antiarrhythmic activity, N-propionylprocainamide (NPPA) may be less harmful than PA, and NAPA. Effects of milimolarly equivalent doses of NPPA, NAPA and PA on the cardiac output and the stroke volume index, as well as on the coronary blood flow were investigated in rabbits by the radioisotope method. The obtained results were subjected to statistical analysis. NPPA was found to display no depressive action on the function of the left ventricle. Moreover, it was found to improve the coronary blood flow in rabbits.

Acecainide↗
PubMed1988

Clinical use of sustained-release procainamide in treatment of cardiac arrhythmias.

Although procainamide has been available, and used, in the treatment of atrial and ventricular arrhythmias for approximately thirty years, its short half-life has made it less than optimal for long-term arrhythmia management in ambulatory patients. Currently available sustained-release preparations provide the same therapeutic benefit with a more tolerable dosage schedule. The pharmacology of procainamide and its basic electrophysiologic properties, dosage schedules, and toxicity are discussed. Finally, the current indications for its use are reviewed.

Arrhythmias, Cardiac↗
PubMed1979

Procainamide-induced agranulocytosis and thrombocytopenia.

Procainamide therapy has frequently been reported as a cause of agranulocytosis, but severe thrombocytopenia associated with the use of this drug has been noted only once. We report a case of simultaneously occurring agranulocytosis and profound thrombocytopenia in a patient receiving procainamide hydrochloride. Different mechanisms appeared to be responsible for the two cytopenias.

Aged↗
PubMedDate not supplied

Covalent binding of procainamide in vitro and in vivo to hepatic protein in mice.

Procainamide (PA) formed reactive metabolites capable of covalently binding to protein both in vivo and in vitro. The in vitro covalent binding of PA to washed hepatic microsomal protein prepared from control male mice was dependent upon mixed-function oxidase activity. The binding was proportional with time and protein concentration. Glutathione and SKF 525-A inhibited the in vitro covalent binding by 88 and 51%, respectively. The addition of NaF to the incubation medium produced a concentration-dependent decrease in covalent binding. Covalent binding of N-acetylprocainamide in vitro was 90% less than that of procainamide and was not increased by NaF. The in vivo covalent binding of PA to hepatic protein in male mice was increased with phenobarbital and 3-methylcholanthrene pretreatment, resulting in increase in binding of 29 and 56%, respectively, compared to control mice. Pretreatment of mice with SKF 525-A inhibited binding by 39%. Depletion of hepatic glutathione with diethyl maleate pretreatment increased the amount of covalent binding in vivo. Bioactivation of PA by hepatic microsomal enzymes in the mouse produces a metabolite capable of covalent interactions with cellular macromolecules.

Acecainide↗
PubMed1981

Studies on a circulating anticoagulant in procainamide-induced lupus erythematosus.

Circulating anticoagulant activity that had at least two distinct mechanisms--one directed against factor XII and one directed against blood thromboplastin (prothrombin activator complex)--developed in a patient with clinical and laboratory evidence of procainamide hydrochloride-induced systemic lupus erythematosus. The anticoagulant activity behaved as a gamma-globulin in chromatographic and electrophoretic analyses, with the majority of activity behaving as an IgM immunoglobulin. Despite markedly abnormal coagulation study results, no clinical bleeding occurred. Anticoagulant activity paralleled clinical and laboratory evidence of the inflammatory disease and improved on discontinuance of procainamide therapy.

Aged↗
PubMed1978

Circulating thrombin time anticoagulant in a procainamide-induced syndrome.

Circulating anticoagulants are unusual in drug-induced syndromes. We evaluated the prolonged thrombin time of plasma from a patient with a procainamide-induced syndrome. This defect was shown to be due to a circulating anticoagulant that was not of fibrin or fibrinogen origin and that prolonged thrombin and reptilase clotting times of plasma. Subclinical doses of heparin sodium induced hemorrhagic manifestations in this patient. Following cessation of heparin therapy, the circulating anticoagulant persisted but the bleeding tendency abated. All clinical and laboratory manifestations of this syndrome abated gradually following cessation of procainamide therapy.

Aged↗
PubMed1984

Cerebellar ataxia due to procainamide toxicity.

It has become appreciated that drug levels of procainamide hydrochloride needed to suppress inducible ventricular tachycardia by programmed ventricular stimulation exceed the previously published therapeutic range. Cerebellar ataxia developed acutely in a patient receiving high-dose procainamide. This was associated with a marked increase in the serum drug level. Resolution occurred within three days after drug therapy was discontinued.

Administration, Oral↗
PubMed1983

Low-dose procainamide: low risk of complications with long-term use.

The incidence of procainamide-induced drug reactions was studied prospectively in 55 patients receiving long-term therapy with a mean duration of 23 months. New symptoms that occurred in 13 patients after the drug was started were similar to complaints presented by 25 patients before the medication was started. Duration of therapy was positively correlated with new symptom occurrence (P < .05) but not with age, sex, dose, or dose interval. Other concomitant drugs did not influence the results. Antideoxyribonucleoprotein antibodies were positive in 27 patients (55 percent) and in seven of 13 with new symptoms; female sex (P < .05) and increasing age (P < .05) favored a positive test. Anti-DNA antibodies were not found in any patients. Procainamide, at a mean dose of 1.5 g/day, was judged to be therapeutically effective by the clinic staff independent of this study; the drug was not discontinued in any patient because of the severity of symptoms.

Adult↗
PubMed1978

Pharmacokinetic and pharmacodynamic studies of procainamide given intermittently intravenously in patients with severe ventricular arrhytmias.

In 15 patients with coronary heart disease and ventricular arrhythmias 100 mg of procainamide was given intravenously every 5 min until arrhythmia was abolished, or the patient received 1000 mg of the drug, or side-effects appeared. Then patients were placed on oral maintenance therapy 3 or 4 g daily according to their weight. In 13 out of 15 patients arrhythmia was completely suppressed after intravenous injections of the drug. Plasma procainamide concentrations, including N-acetylprocainamide levels in some patients, were monitored and a therapeutic range of 6.3--10.3 microgram/ml for intravenous therapy was found. ECG intervals changes, slowing of heart rate and decrease in systolic and diastolic blood pressure were seen but no serious side-effects were observed. The significance of monitoring plasma drug concentrations, including levels of N-acetylprocainamide during prolonged maintenance therapy, have been discussed.

Adult↗
PubMedDate not supplied

Crithidia luciliae assay for antibodies to native DNA in procainamide-induced lupus erythematosus.

Sera from 49 patients with procainamide-induced lupus erythematosus or circulating antinuclear antibodies were found to be negative for antibodies to native DNA by the CL immunofluorescence assay. This finding suggests that the CL assay is helpful in discriminating between procainamide-induced and naturally occurring systemic lupus erythematosus. The results further confirm the relatively high degree of specificity of the CL assay for SLE.

Adult↗
PubMed1978

Bone marrow granulomas and neutropenia associated with procainamide. Report of a case.

Bone marrow granulomas and neutropenia occurred in a 77-year-old man following the ingestion of procainamide hydrochloride for 50 days. Although neutropenia has occasionally occurred following procainamide therapy, granulomas in the bone marrow have not previously been associated with the use of this drug. There was no other apparent agent that could have been responsible for the granulomas. Eighteen days after administration of the drug had been discontinued, the WBC count returned to normal and there were no granulomas present in the bone marrow.

Aged↗
PubMed1978

[Hemodynamic effects of disopyramide and procainamide in open-chest animals].

Hemodynamic effects of two antiarrhythmic agents, disopyramide and procainamide, have been evaluated in anesthetized open-chest healthy pigs after random administration. At therapeutic plasma concentrations none of these agents proved to have deleterious hemodynamic effects. The most important action was observed after disopyramide infusion and consisted in significant bradycardia which confirmed the known effect on sinus node automaticity of the drug. Left ventricular dp/dt, an index of cardiac contractility, was unchanged after infusion of both drugs. On the ECG intervals, only procainamide provoked a significant prolongation of QTc. It is concluded that at therapeutic dosage disopyramide does not present deleterious hemodynamic effects in animals and proves to be a valid alternative to other traditional antiarrhythmic agents.

Animals↗
PubMed1993

Effects of procainamide, tocainide and phenytoin on guinea pig cardiac mitochondrial ATPase activity.

The effects of three class I antiarrhythmic drugs procainamide, tocainide and phenytoin on undamaged myocardial mitochondrial ATPase [ATP: phosphohydrolase EC 3.6.1.3] activity were evaluated in guinea pig heart preparations. Tocainide inhibited the ATPase activity in the range of 1.0 nM-500 mM, exhibiting IC20 and IC50 values of 9.4 +/- 0.7 microM and 5.2 +/- 0.4 mM, while procainamide exhibited significant (p < 0.05) inhibitory effect only at concentrations above 1.0 mM with IC20 and IC50 values of 35.4 +/- 2.7 mM and 90.8 +/- 3.7 mM, respectively. On the other hand, phenytoin inhibited the enzyme by 17% and 8% at 1.0 nM and 1.0 microM respectively, while it stimulated it at higher concentrations, thereby increasing its activity by 10%, 57% and 227% at 10, 100, 1000 microM, respectively. The inhibitory actions of these drugs are probably related to their lipophilicity and membrane stabilizing activity, while the stimulatory effect of phenytoin suggests some specific interaction with some component(s) of the oxidative phosphorylation or respiratory chain.

Adenosine Triphosphatases↗
PubMedDate not supplied

The influence of selected general anesthetics on pharmacokinetic parameters of some antiarrhythmic drugs in rabbits. Part I. Procainamide and its active metabolite-N-acetylprocainamide.

The influence of general anesthesia with thiopental (10 mg/kg), ketamine (4 mg/kg), propofol (10 mg/kg) or pentobarbital (20 mg/kg) on the pharmacokinetics of procainamide (13 mg/kg) and its active metabolite-N-acetylprocainamide was studied in rabbits. The general anesthesia with those drugs caused only the slight changes in procainamide pharmacokinetics, namely changing volume of distribution, penetration rate constants between central and peripheral compartments. However, the following main changes in N-acetylprocainamide (metabolite) pharmacokinetic parameters were found: 1) increase of the penetration rate constants between the compartments and mean residence time during propofol anesthesia 2) prolongation of the mean residence time during thiopental anesthesia 3) increase of mean residence time of N-acetylprocainamide during anesthesia with ketamine, pentobarbital or propofol.

Acecainide↗