Acecainide
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Anti-Arrhythmia Agents
Agents used for the treatment or prevention of cardiac arrhythmias. They may affect the polarization-repolarization phase of the action potential, its excitability or refractoriness, or impulse conduction or membrane responsiveness within cardiac fibers. Anti-arrhythmia agents are often classed into four main groups according to their mechanism of action: sodium channel blockade, beta-adrenergic blockade, repolarization prolongation, or calcium channel blockade.
Procaine
Prediction of N-acetylprocainamide disposition kinetics in rat by combination of gamma variate and physiological pharmacokinetic model. (1/13)
Clearances and tissue/blood drug concentration ratios of N-acetylprocainamide (NAPA) in rats were determined. The clearances of NAPA in rat blood, liver, and kidney were 13.1, 4.88, and 8.24 ml.kg-1.min-1, respectively. Disposition kinetics of NAPA in rats was predicted with combination of gamma variate and physiological pharmacokinetic model. Equation for estimating the concentration of NAPA in rat blood following iv NAPA 40 mg.kg-1 was C = 55.06t(-0.220) exp(-0.00713t). Using r2 value as a criterion, we found a good agreement between predicted and observed concentrations in blood, lung, small intestine, heart, brain, and skin. (+info)Effects of antiarrhythmic drugs on phospholipid metabolism in Jurkat T cells. The potassium channel blocker, clofilium, specifically increases phosphatidylserine synthesis. (2/13)
Five antiarrhythmic drugs (bretylium, clofilium, propranolol, N-acetylprocainamide and amiodarone) were tested for their ability to modify phospholipid metabolism in Jurkat T lymphocytes. The five drugs, decreased in a dose-dependent mode the biosynthesis of both phosphatidylcholine and phosphatidylethanolamine, this effect was essentially due to impairment of either choline or ethanolamine uptake by the cells. The efficiency of the drugs to inhibit phosphatidylcholine and phosphatidylethanolamine synthesis was in the order: clofilium greater than amiodarone much greater than propranolol = bretylium much greater than N-acetylprocainamide. The IC50 varied from 3-5 microM for clofilium to greater than 200 microM for N-acetylprocainamide. In contrast, only clofilium, a voltage-gated K(+)-channel blocker, was able to increase phosphatidylserine synthesis with an EC50 = 50 microM. The effect of clofilium on phosphatidylserine synthesis thus mimics the effect of three other K(+)-channel blockers, quinine, 4-aminopyridine and tetraethylammonium, suggesting close relationships between phosphatidylserine synthesis and K+ channel activity. (+info)Levofloxacin and ciprofloxacin decrease procainamide and N-acetylprocainamide renal clearances. (3/13)
Ten healthy adults participated in a randomized, crossover drug interaction study testing procainamide only, procainamide plus levofloxacin, and procainamide plus ciprofloxacin. During levofloxacin therapy, most procainamide and N-acetylprocainamide (NAPA) pharmacokinetic parameters, including decreased renal clearances and renal clearance/creatinine clearance ratios, changed (P < 0.05). During ciprofloxacin treatment, only procainamide and NAPA renal clearances decreased significantly. (+info)Application of a generic physiologically based pharmacokinetic model to the estimation of xenobiotic levels in human plasma. (4/13)
Estimation of xenobiotic kinetics in humans frequently relies upon extrapolation from experimental data generated in animals. In an accompanying paper, we have presented a unique, generic, physiologically based pharmacokinetic model and described its application to the prediction of rat plasma pharmacokinetics from in vitro data alone. Here we demonstrate the application of the same model, parameterized for human physiology, to the estimation of plasma pharmacokinetics in humans and report a comparative evaluation against some recently published predictive methods that involve scaling from in vivo animal data. The model was parameterized through an optimization process, using a training set of in vivo data taken from the literature, and validated using a separate test set of published in vivo data. On average, the vertical divergence of the predicted plasma concentrations from the observed data, on a semilog concentration-time plot, was 0.47 log unit. For the training set, more than 80% of the predicted values of a standardized measure of the area under the concentration-time curve were within 3-fold of the observed values; over 70% of the test set predictions were within the same margin. Furthermore, in terms of predicting human clearance for the test set, the model was found to match or exceed the performance of three published interspecies scaling methods, all of which showed a distinct bias toward overprediction. We conclude that the generic physiologically based pharmacokinetic model, as a means of integrating readily determined in vitro and/or in silico data, is potentially a powerful, cost-effective tool for predicting human xenobiotic kinetics in drug discovery and risk assessment. (+info)Procainamide, but not N-acetylprocainamide, induces protein free radical formation on myeloperoxidase: a potential mechanism of agranulocytosis. (5/13)
(+info)More-sensitive enzyme-multiplied immunoassay technique for procainamide and N-acetylprocainamide in plasma, serum, and urine. (6/13)
A commercially available (Syva Co.) enzyme-multiplied immunoassay technique (EMIT) for the quantitative determination of procainamide (PA) and N-acetylprocainamide (NAPA) was modified to allow automated quantitative analysis of approximately 100 samples per day, in a working range of 0.1 to 2.0 micrograms/mL. Such a test was needed to evaluate the pharmacokinetic characteristics of controlled-release dosage forms characterized by long half-lives at low plasma concentration. Analytical recovery of PA and NAPA from serum, plasma, and urine was satisfactory, but at extreme ratios for PA:NAPA the accuracy of determining the lower-concentration component became unsatisfactory. In fact, however, we found no such ratios in 5400 clinical samples assayed by this procedure. (+info)Metabolites of procainamide and practolol inhibit complement components C3 and C4. (7/13)
Drug-induced systemic lupus erythematosus arises from toxic side-effects of administration of hydralazine, isoniazid, procainamide and practolol. Hydralazine and isoniazid are nucleophilic drugs and inhibit the covalent binding reaction of complement components, C3 and C4, an effect likely to lead to deposition of immune complexes (a feature of systemic lupus erythematosus). Procainamide and practolol do not themselves inhibit C3 and C4. A range of metabolites and putative metabolites of procainamide and practolol were synthesized, and tested for their ability to inhibit the covalent binding reactions of C3 and C4. The highly nucleophilic hydroxylamine metabolite of procainamide was strongly inhibitory in both tests, as was a putative hydroxylamine metabolite of practolol. These studies indicate a potential role for the hydroxylamine metabolites in mediating the toxic side-effects of procainamide and practolol, and emphasize the need for adequate measurements of hydroxylamine metabolites in human tissue. (+info)Four fluorescence polarization immunoassays for therapeutic drug monitoring evaluated. (8/13)
We evaluated four fluorescence polarization immunoassays--those for phenytoin, procainamide, N-acetylprocainamide (NAPA), and quinidine--from Roche Diagnostic Systems, done in the Cobas Bio FP centrifugal analyzer. The assays for phenytoin, NAPA, and quinidine demonstrated a linear response over the expected ranges of concentrations, and analytical recovery of test drug added to drug-free sera was greater than 90%. However, recovery in the procainamide assay was poor (69-82%) for samples containing greater than 8 mg/L, owing to nonlinearity. Results of method-comparison studies of the four assays paralleled the recovery studies, although the quinidine assay demonstrated a bias (1.0 mg/L higher) when compared with EMIT (Syva). The precision of the phenytoin assay was acceptable at all concentrations tested (total CV less than 7.0%). Imprecision of the other assays was significant at certain concentrations: total CV greater than 10.0% at subtherapeutic values for NAPA and quinidine, and greater than 9.0% for low (2.4 mg/L) and moderate concentrations (9.6 mg/L) of procainamide. Interferences were not significant for hemolyzed, icteric, or lipemic specimens or for specimens with added drug metabolites. The calibration curves for all four assays had good stability (greater than 60 days). (+info)Procainamide, but not N-Acetylprocainamide, Induces Protein Free Radical Formation on Myeloperoxidase: A Potential Mechanism of...
Acecainide - Wikipedia
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List of MeSH codes (D02)
... acecainide MeSH D02.241.223.100.054.055.105 - benzocaine MeSH D02.241.223.100.054.055.650 - procainamide MeSH D02.241.223.100. ...
List of drugs: Ac
... acecainide (INN) acecarbromal (INN) aceclidine (INN) aceclofenac (INN) acedapsone (INN) acediasulfone (INN) acedoben (INN) ...
Napa
... acecainide), an anti-arrhythmic heart drug NAPA Auto Parts, an American retailers' cooperative National Academy of Public ...
Acecainide
Some acecainide can convert to procainamide. The deacetylation clearance of acecainide is 0.39 L/h compare to a total NAPA ... acecainide can cause cardiac toxicity that effects in torsades de pointes. Also acecainide can decrease renal function when it ... Acecainide is considered comparable in activity to its parent compound; however, acecainide levels will vary widely. Serum ... However, hypotension has been reported in association with a rapid injection of acecainide. In animals, acecainide has positive ...
Acecainide - Wikipedia
Some acecainide can convert to procainamide. The deacetylation clearance of acecainide is 0.39 L/h compare to a total NAPA ... acecainide can cause cardiac toxicity that effects in torsades de pointes. Also acecainide can decrease renal function when it ... Acecainide is considered comparable in activity to its parent compound; however, acecainide levels will vary widely. Serum ... However, hypotension has been reported in association with a rapid injection of acecainide. In animals, acecainide has positive ...
Fluoxetine (Oral Route) Before Using - 妙佑医疗国际
Although certain medicines should not be used together at all, in other cases two different medicines may be used together even if an interaction might occur. In these cases, your doctor may want to change the dose, or other precautions may be necessary. When you are taking this medicine, it is especially important that your healthcare professional know if you are taking any of the medicines listed below. The following interactions have been selected on the basis of their potential significance and are not necessarily all-inclusive.. Using this medicine with any of the following medicines is not recommended. Your doctor may decide not to treat you with this medication or change some of the other medicines you take.. ...
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This medicine should be used only for problems being treated by your doctor or conditions listed in the package directions. Check with your doctor before using it for other problems, especially if you think that an infection may be present. This medicine should not be used to treat certain kinds of skin infections or serious problems, such as severe burns.. Read the package label very carefully to see if the product contains any alcohol. Alcohol is flammable and can catch on fire. Do not use any product containing alcohol near a fire or open flame, or while smoking. Also, do not smoke after applying one of these products until it has completely dried.. If you are using this medicine on your face, be very careful not to get it in your eyes, mouth, or nose. If you are using an aerosol or spray form of this medicine, do not spray it directly on your face. Instead, use your hand or an applicator (for example, a sterile gauze pad or a cotton swab) to apply the medicine.. For patients using butamben: ...
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Haldol Decanoate (Intramuscular) - Questiontime.info
It is very important that your doctor check your progress while you receive this medicine to allow for changes in your dose and help reduce any unwanted effects.. Do not stop receiving Haldol® suddenly without asking your doctor. You may need to slowly decrease your dose before stopping it completely.. This medicine may cause serious allergic reactions (eg, anaphylaxis, angioedema, dermatitis exfoliative), which can be life-threatening and require immediate medical attention. Tell your doctor right away if you have a cracks in the skin, loss of heat from the body, rash, itching, hoarseness, red, swollen skin, scaly skin, trouble breathing, trouble swallowing, or any swelling of your hands, face, or mouth after receiving this medicine.. Contact your doctor as soon as possible if you have chest pain or discomfort, a fast heartbeat, trouble with breathing, or fever and chills. These may be symptoms of a very serious problem with your heart.. This medicine may cause tardive dyskinesia (a movement ...
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Although certain medicines should not be used together at all, in other cases two different medicines may be used together even if an interaction might occur. In these cases, your doctor may want to change the dose, or other precautions may be necessary. When you are taking this medicine, it is especially important that your healthcare professional know if you are taking any of the medicines listed below. The following interactions have been selected on the basis of their potential significance and are not necessarily all-inclusive.. Using this medicine with any of the following medicines is not recommended. Your doctor may decide not to treat you with this medication or change some of the other medicines you take.. ...
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Bugaev N, Bhattacharya B, Chiu WC, Como JJ, Cripps MW, Ferrada P, Gelbard RB, Gondek S, Kasotakis G, Kim D, Mentzer C, Robinson BRH, Salcedo ES, Yeh DD. Promotility agents for the treatment of ileus in adult surgical patients: A practice management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg. 2019 10; 87(4):922-934 ...
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MeSH Browser
Acecainide Hydrochloride Narrower Concept UI. M0000194. Registry Number. B9K738KX14. Terms. Acecainide Hydrochloride Preferred ... Acecainide Hydrochloride Acecainide Monohydrochloride Acetylprocainamide N-Acetylprocainamide Pharm Action. Anti-Arrhythmia ... Acecainide Preferred Term Term UI T000367. Date01/01/1999. LexicalTag NON. ThesaurusID ... Acecainide Preferred Concept UI. M0000193. Registry Number. 910Q707V6F. Related Numbers. 32795-44-1. 34118-92-8. B9K738KX14. ...
MeSH Browser
Acecainide Hydrochloride Narrower Concept UI. M0000194. Registry Number. B9K738KX14. Terms. Acecainide Hydrochloride Preferred ... Acecainide Hydrochloride Acecainide Monohydrochloride Acetylprocainamide N-Acetylprocainamide Pharm Action. Anti-Arrhythmia ... Acecainide Preferred Term Term UI T000367. Date01/01/1999. LexicalTag NON. ThesaurusID ... Acecainide Preferred Concept UI. M0000193. Registry Number. 910Q707V6F. Related Numbers. 32795-44-1. 34118-92-8. B9K738KX14. ...