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American Heart Journal Dec 1985
Topics: Acecainide; Humans; Male; Metabolic Clearance Rate; Middle Aged; Peritoneal Dialysis, Continuous Ambulatory; Procainamide
PubMed: 2416212
DOI: 10.1016/0002-8703(85)90034-1 -
European Journal of Clinical... Dec 1978Procainamide 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...
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.
Topics: Biological Availability; Delayed-Action Preparations; Electrocardiography; Half-Life; Humans; Kinetics; Procainamide
PubMed: 729620
DOI: 10.1007/BF00560459 -
The New Zealand Medical Journal Dec 1967
Topics: Adult; Aged; Antiemetics; Female; Humans; Labyrinth Diseases; Male; Meniere Disease; Middle Aged; Procainamide; Vertigo
PubMed: 5236016
DOI: No ID Found -
The Journal of Pharmacy and Pharmacology Sep 1985The aim of this study was to investigate the possible influence of the time of administration on procainamide and N-acetylprocainamide (NAPA) kinetics in the rat. A...
The aim of this study was to investigate the possible influence of the time of administration on procainamide and N-acetylprocainamide (NAPA) kinetics in the rat. A single 50 mg kg-1 i.p. dose of procainamide was given to Wistar AF SPF adult male rats maintained under controlled environmental conditions (LD: 06.00h-18.00h) at four different fixed times i.e. 10.00, 16.00, 22.00 and 04.00h. Procainamide and NAPA plasma levels were determined by an immunoenzymatic method. Our data showed significant 24 h variation of the following pharmacokinetic parameters: highest elimination half-lives at 10.00h (t1/2 beta = 0.736 +/- 0.020h) for procainamide and at 04.00h (t1/2 beta = 3.55 +/- 0.08h) for NAPA (P less than 0.001); highest apparent volume of distribution at 04.00h for procainamide (Vd = 2.35 +/- 0.17 litre) (P less than 0.05); highest ratio AUC NAPA/AUC procainamide at 04.00h (1.039 +/- 0.056) (P less than 0.001). Procainamide clearance and Cmax and AUC for procainamide and NAPA were not significantly dependent on time of day. These data indicate a 24 h variation in the metabolism of procainamide which is converted to NAPA, the N-acetylation being greatest at 04.00h.
Topics: Acecainide; Animals; Circadian Rhythm; Half-Life; Injections, Intraperitoneal; Kinetics; Male; Procainamide; Rats; Rats, Inbred Strains
PubMed: 2416904
DOI: 10.1111/j.2042-7158.1985.tb05105.x -
The New England Journal of Medicine Dec 1969
Clinical Trial
Topics: Acute Disease; Aged; Arrhythmias, Cardiac; Blood Pressure; Clinical Trials as Topic; Electrocardiography; Female; Heart; Heart Rate; Humans; Lidocaine; Male; Middle Aged; Monitoring, Physiologic; Myocardial Infarction; Placebos; Procainamide
PubMed: 4900236
DOI: 10.1056/NEJM196912042812301 -
The American Journal of Cardiology Jul 1985The efficacy and tolerance of quinidine and procainamide used individually and in combination were studied in 19 patients with frequent ventricular premature complexes...
The efficacy and tolerance of quinidine and procainamide used individually and in combination were studied in 19 patients with frequent ventricular premature complexes (VPCs). During single-drug treatment, the maximum tolerated dose of quinidine without extracardiac dose-related side effects was 1.6 +/- 0.21 g/day and that of procainamide was 4.1 +/- 1.05 g/day. During combination therapy with smaller doses (p less than 0.05) of quinidine (1.16 +/- 0.26 g/day) and procainamide (2.80 +/- 0.98 g/day), no patient had side effects. Before treatment, all patients had frequent (more than 60 per hour) VPCs and 17 had ventricular tachycardia on Holter monitoring. The frequency of VPCs was reduced to 22 +/- 19% with quinidine, 47 +/- 40% with procainamide and 9 +/- 11% with combination therapy (p less than 0.05, combination vs procainamide or quinidine alone). Individually, an effective regimen (more than 83% reduction of VPCs and abolition of ventricular tachycardia) was found in 5 patients (26%) receiving quinidine alone at maximal tolerated dose, in 4 (21%) receiving procainamide alone at maximal tolerated dose, and in 14 (74%) receiving combination therapy (p less than 0.01 vs quinidine or procainamide). Thus, the antiarrhythmic effects of quinidine and procainamide are additive. When quinidine or procainamide are additive. When quinidine or procainamide is ineffective because dose-related extracardiac side effects limit the maximal tolerated dose, combination therapy in smaller and tolerable doses avoids side effects and is more effective than either drug alone at the maximal tolerated dose.
Topics: Adult; Aged; Ambulatory Care; Arrhythmias, Cardiac; Drug Therapy, Combination; Drug Tolerance; Electrocardiography; Female; Heart Ventricles; Humans; Male; Middle Aged; Procainamide; Quinidine
PubMed: 4014046
DOI: 10.1016/0002-9149(85)90571-5 -
The American Journal of Cardiology Jan 1979Thirty-four patients who were resistant to conventional doses of lidocaine received procainamide intravenously according to a pharmacokinetically designed two infusion...
Thirty-four patients who were resistant to conventional doses of lidocaine received procainamide intravenously according to a pharmacokinetically designed two infusion technique. A mean peak serum concentration of 7.1 mg/liter was achieved with an average loading dose of 989 mg administered over 1 hour. A mean steady state serum concentration of procainamide of 6.5 mg/liter was achieved with a mean dose of 64.4 mg/kg body weight for the first 24 hours of treatment. Dose, renal impairment, the degree of congestive heart failure and acetylator status influenced the steady state serum concentration of procainamide. Dangerous ventricular arrhythmias were abolished in 74% of the patients at a steady state level of 6.9 +/- 3.7 mg/liter (mean +/- standard deviation). Nonresponders to procainamide had a mean steady state serum concentration of procainamide of 4.2 +/- 2.1 mg/liter (P less than 0.05). Systolic and diastolic blood pressures decreased moderately (10 and 8%, respectively), and heart rate decreased 11%. The infusion was interrupted in one patient because of hypotension. The duration of electrocardiographic conduction intervals was increased slightly in some patients. It is concluded that procainamide administered by this two infusion method is effective and well tolerated by most patients.
Topics: Arrhythmias, Cardiac; Blood Pressure; Drug Evaluation; Electrocardiography; Heart Conduction System; Heart Rate; Humans; Infusions, Parenteral; Myocardial Infarction; Procainamide
PubMed: 758776
DOI: 10.1016/0002-9149(79)90051-1 -
Journal of Pharmaceutical Sciences Dec 1975The relationship between serum and stimulated, mixed saliva concentrations of procainamide was determined in 12 chronically medicated patients. Samples were obtained at...
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.
Topics: Humans; Hydrogen-Ion Concentration; Procainamide; Saliva; Time Factors
PubMed: 1514
DOI: 10.1002/jps.2600641226 -
Circulation Research Aug 1991In experimental animals, procainamide causes hypotension and reductions in efferent vasoconstrictor sympathetic outflow that may result from ganglionic blockade or... (Comparative Study)
Comparative Study
In experimental animals, procainamide causes hypotension and reductions in efferent vasoconstrictor sympathetic outflow that may result from ganglionic blockade or central nervous system sympathetic inhibition. To test the hypothesis that procainamide decreases sympathetic nerve activity (SNA) in humans, we recorded postganglionic SNA in seven normal subjects in the baseline state and during infusions of procainamide HCl at 50 mg/min (loading) and 8 mg/min (maintenance). At the end of the loading infusion, mean arterial pressure (MAP) had decreased from 88.5 +/- 2.4 (mean +/- SEM) to 81.5 +/- 3.2 mm Hg (p less than 0.05), central venous pressure from 6.7 +/- 0.7 to 5.4 +/- 0.9 mm Hg (p less than 0.05), forearm vascular resistance (FVR) from 28 +/- 4.8 to 22.3 +/- 5.1 resistance units (p less than 0.05), and SNA from 259 +/- 47 to 94 +/- 26 units/min (p less than 0.05). These changes persisted during the maintenance infusion. Increased levels of SNA, FVR, and MAP provoked by the cold pressor test were reduced significantly by intravenous procainamide. In eight other subjects, intravenous procainamide HCl (15 mg/kg at 50 mg/min) caused dose-dependent inhibition of SNA that reversed as blood concentrations fell during drug washout. To determine if procainamide causes direct vasodilation, in nine subjects, graded infusions were delivered into the brachial artery at doses that produced no systemic effect. Ipsilateral FVR tended to increase during local intra-arterial infusion of procainamide. These data show that intravenous procainamide causes hypotension, vasodilation, and sympathetic withdrawal. Vasodilation does not result from a direct vasorelaxant effect of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)
Topics: Adult; Blood Pressure; Cold Temperature; Heart Rate; Hemodynamics; Humans; Hypotension; Infusions, Intra-Arterial; Infusions, Intravenous; Male; Procainamide; Sympathetic Nervous System; Vasodilation
PubMed: 1860187
DOI: 10.1161/01.res.69.2.501 -
American Journal of Hospital Pharmacy Nov 1979
Topics: Drug Stability; Glucose; Procainamide; Sodium Chloride; Solutions; Water
PubMed: 517523
DOI: No ID Found