Antiarrhythmic potency of N‐acetylprocainamide

Elson, James J.; Strong, John M.; Lee, Woong-Ku; Atkinson, Arthur J.

doi:10.1002/cpt1975172134

Cited by 131 publications

(42 citation statements)

References 2 publications

(2 reference statements)

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“…A similar relationship between the occurrence of systemic lupus erythematosus and slow acetylation phenotype has been reported for patients receiving procainamide (Henningsen, Cederberg, Hanson & Johansson, 1975). In addition, it has been suggested that the N-acetylprocainamide may make a significant contribution to the antiarrhythmic effect resulting from procainamide administration (Elson, Strong, Lee & Atkinson, 1975). Isoniazide-related hepatic injury is associated with rapid drug acetylation and probably hepatotoxicity of the drug metabolites (Mitchell, Zimmerman, Ishak, Thorgeirsson, Timbrell, Snodgrass & Nelson, 1976).…”

Section: Discussionmentioning

confidence: 57%

Acebutolol metabolite plasma concentration during chronic oral therapy.

Winkle¹,

Meffin²,

Ricks³

et al. 1977

Brit J Clinical Pharma

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1We have measured the plasma concentration of acebutolol and a major metabolite in patients on chronic oral therapy with this drug, using a new assay, specific for each species. Our study suggests: 2 The acetyl metabolite was present in concentrations greater than those of acebutolol at all times during the dosing interval in all seven subjects. 3 The ratio of the mean steady-state plasma concentrations of the acetyl metabolite to unchanged acebutolol was 2.7 + 1.0. 4 Previous studies using non-specific methods that measure plasma concentrations of the acetyl metabolite and acebutolol as a single species cannot be used to determine pharmacokinetic parameters or to provide reliable correlations of plasma drug concentration with effect. 5 Future studies determining plasma concentration of acebutolol should take this metabolite into account.6 Further work will be necessary to determine the metabolite's contribution to acebutolol's effects in man.

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Section: Discussionmentioning

confidence: 57%

Acebutolol metabolite plasma concentration during chronic oral therapy.

Winkle¹,

Meffin²,

Ricks³

et al. 1977

Brit J Clinical Pharma

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“…From clinical and pharmacological considerations, KochWeser (1971) has advocated that procainamide should be administered in three hourly doses. However, Biggar (1972) reports satisfactory control of arrhythmias with six hourly administration, perhaps due to anti-arrhythmic effect of the major metabolite -N acetylprocainamide -which has a substantially longer half-time in the plasma than the parent compound (Elson, Strong, Lee & Atkinson, 1975). In the present study three hourly administration was the exception (12%) rather than the rule: the most frequent pattern of administration being 4-5 times daily (40% of recipients).…”

Section: Methodsmentioning

confidence: 40%

Adverse Reactions to Procainamide

1977

Inpharma

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“…NAPA, the principal metabolite of procainamide in man,9 may not have this toxicity and may become an alternative drug inasmuch as it has antiarrhythmic activity in both animal models4 9, 10 and in patients. 4 Our canine electrophysiologic comparative study of procainamide and NAPA may be useful to compare their cardiac effects and to delineate the possible mechanism of action of NAPA.…”

Section: Discussionmentioning

confidence: 99%

Electrophysiologic comparative study of procainamide and N-acetylprocainamide in anesthetized dogs: concentration-response relationships.

Jaillon¹,

Winkle²

1979

Circulation

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SUMMARY The electrophysiologic effects of n-acetylprocainamide (NAPA) and procainamide (PA) were compared in 14 chloralose-anesthetized dogs using intracardiac electrography and programmed stimulation. With five successive sequences of an intravenous bolus followed by a 45-minute infusion, plasma concentrations (Cp) ranged from 1.8 ± 0.1 to 32 ± 2 g/ml for PA and from 8.2 ± 0.3 to 125 i 7 ,ug/ml for NAPA. In 6, 1979. between the electrophysiologic effects and plasma drug concentration (Cp).In the present study we compared the electrophysiologic properties of NAPA and procainamide in closed-chest, anesthetized dogs using His bundle electrography and programmed electrical stimulation. The effects of the drugs were examined over a wide range of Cps achieved by different intravenous infusion rates. Methods General ProceduresSeventeen mongrel dogs of either sex (19-31 kg, average 24 kg) were anesthetized with morphine sulfate 2 mg/kg subcutaneously, followed 30 minutes later by a-chloralose 200 mg/kg intravenously (4% solution in polyethylene glycol and distilled water). The dogs were intubated with a cuffed endotracheal tube. Artificial ventilation was maintained with a Harvard respirator pump using humidified room air. A large polyethylene catheter was inserted into the left femoral artery to monitor the systemic arterial pressure using a Statham P23Db transducer. The mean arterial blood pressure was calculated using the formula BP = diastolic pressure + 1/3 of the pulse pressure.'5 The same catheter was used to draw blood samples for arterial blood gas analysis using a Corning model 165 blood gas analyzer. Depth and rate of respiration were adjusted to maintain an arterial Po2 over 72 mm Hg and pH between 7.35 and 7.44 throughout the experiment.A catheter was placed in the left femoral vein for administration of additional anesthetic, which was given hourly (10 ml of 4% chloralose solution) to 1385

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Antiarrhythmic potency of N‐acetylprocainamide

Cited by 131 publications

References 2 publications

Acebutolol metabolite plasma concentration during chronic oral therapy.

Acebutolol metabolite plasma concentration during chronic oral therapy.

Adverse Reactions to Procainamide

Electrophysiologic comparative study of procainamide and N-acetylprocainamide in anesthetized dogs: concentration-response relationships.

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