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PubMed1978

The effect of isoniazid and other drugs on the acetylation of procainamide in the intact rat.

The effects of isoniazid (INH), hydralazine, salicylazosulfapyridine, and sulfapyridine on the quantitative disposition of procainamide (PA) in the intact rat were examined. A dose-dependent inhibition of PA acetylation was observed after coadministration of PA with INH via nasogastric intubation. The 24-hr urinary excretion of N-acetylprocainamide was noted to decline in the presence of INH whereas that of the unchanged drug exhibited a coincident rise. A reduction in the systemic clearance of PA and a prolongation in its half-life of elimination was also observed. INH increased PA hepatic levels and decreased N-acetylprocainamide hepatic content. In contrast hydralazine affects not only PA acetylation but also its absorption rate and transformation by other metabolic pathways. Salicylazosulfapyridine did not affect PA acetylation whereas high doses of sulfaphridine did.

Acetylation↗
PubMed1995

The discordant influences of infarct healing on the electrophysiologic effects of procainamide and N-acetylprocainamide.

Ischemic zone refractoriness and conduction delay respond differently to infarct healing and, hypothetically, may exert discordant influences on the electrophysiologic action of different classes of antiarrhythmic drugs. This study evaluated the influence of infarct healing on the electrophysiologic effects of procainamide (PA) and N-acetylprocainamide (NAPA) in a sedated, closed-chest canine model with a healing anterior wall myocardial infarction, indwelling myocardial electrodes and inducible sustained ventricular tachyarrhythmias (VT). Infarct zone refractory periods, conduction times and the inducibility of VT were tested at base line and during infusion of PA or NAPA in a crossover study design at 1, 4 and 8 weeks of infarct healing. Data were presented as the percent magnitude of change from base line induced by drug. The magnitude of change during PA infusion in infarct zone refractory periods, but not conduction times, decreased during infarct healing (P < .001). The magnitude of change in refractory period and conduction time during NAPA was not significantly altered by the stage of myocardial infarction healing. At week 1, PA prevented inducible VT in 9 of 14 animals vs. 3 of 15 during NAPA infusion (P < .05). At weeks 4 and 8 there was no significant difference in VT suppression between PA and NAPA. We conclude that the stage of infarct healing can selectively influence the response of the infarct zone to the effects of PA, but not NAPA. This discordant effect may be class-specific. These data may have important implications for the management of lethal ventricular arrhythmias soon after myocardial infarction.

Acecainide↗
PubMed1977

Measurement of procainamide and N-acetylprocainamide in serum by high-performance liquid chromatography.

We measured procainamide (I) and its metabolite, N-acetylprocainamide (II), in human serum samples by solvent extraction, high-performance liquid chromatography on a reverse phase column, and detection at 280 nm, with use of external standards. The method requires 0.2 ml of serum and is sensitive to 0.3 mg of I and 0.6 mg of II per liter of serum, with intra-assay standard deviations of 0.22 and 0.24 mg/liter, respectively, at 5 mg/liter (N=10) and inter-assay standard deviations of 0.63 and 0.81 mg/liter, respectively, at 7.5 mg/liter (CV 8.4 and 10.5%, respectively, n = 20). Concentrations measured by high-performance liquid chromatography and by an established fluorescence technique correlated well (r = 0.98 for I and 0.97 for II). No interfering substances were found in 20 randomly selected sera from patients receiving a large number of other drugs. Of the pure drug substances tested only sulfathiazole interfered with the assay of II. The method is therefore suitable for routinely monitoring these compounds in serum in a clinical laboratory. The high concentrations of the metabolite in a significant number of patients demonstrate the need to consider it as well as the parent drug as guides in optimizing dosage regiments for I.

Chromatography, High Pressure Liquid↗
PubMed1977

Determination of plasma procainamide and N-acetylprocainamide concentration by high-pressure liquid chromatography.

We describe a routine method for determining concentrations of the antiarrhythmic drug procainamide and its active metabolite, N-acetylprocainamide, in plasma. A simple extraction of 1.0 ml of plasma is followed by separation and chromatographic analysis by use of a column containing microparticulate silica. p-nitro-N-(2-diethylaminoethyl)benzamide hydrochloride was synthesized and used as the internal standard. Total chromatographic time is only 7 min. The day-to-day CV during three months of daily use was less than 4% of the mean for each compound, and we saw no deterioration in column performance during this time. Phenobarbital, phenytoin, lidocaine, primidone, methsuximide, quinidine, and their metabolites do not interfere.

Anti-Arrhythmia Agents↗
PubMed1996

Effect of procainamide on pulmonary thromboembolism and platelet malondialdehyde in mice.

AIM: To study the effect of procainamide (PA) on pulmonary thromboembolism, platelet malondialdehyde (MDA) level and platelet aggregation induced by collagen and adrenaline. METHODS: Pulmonary thromboembolism, 2-thiobarbituric acid fluorescence micro-determination, conventional microscopic counting, and platelet aggregation test were used. RESULTS: PA (10-20 mg.kg-1) and mannitol (200 mg.kg-1) reduced thrombosis by 30%-75% and 75%, respectively. Thrombocytopenia followed thrombosis increased after the pretreatment of PA and mannitol. MDA decreased by both of them in vivo. In vitro, PA inhibited platelet aggregation and MDA production induced concentration-dependently by collagen and adrenaline. CONCLUSION: Inhibition of PA on pulmonary thromboembolism is involved in the decrease of platelet aggregation and MDA production.

Animals↗
PubMed1990

[Combined pharmacokinetic--pharmacodynamic model analysis of N-acetyl procainamids following intravenous infusion in rabbits].

The pharmacokinetic and pharmacodynamic profiles of N-acetyl procainamide were analyzed by integrated PK-PD model following intravenous infusion to rabbits. No significant differences between the PK parameters estimated from iv administration and intravenous infusion were found. However, two of the PD parameters were shown to be significantly different. The values of Emax, Keo, S, EC50 were found to be 120 +/- 13.2 ms, 0.0182 +/- 0.007 min-1, 2.26 +/- 0.93, 6.31 +/- 0.71 microgram/ml respectively following intravenous infusion; the corresponding values following iv administration were 53.6 +/- 2.5 ms, 0.061 +/- 0.017 min-1, 2.19 +/- 0.39, 6.21 +/- 1.74 micrograms/ml respectively.

Acecainide↗