PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Procainamide”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,585 records · Page 88Linked to original sources

Resin hemoperfusion for drug intoxication--an update.

Hemoperfusion through Amberlite XAD-4 resin column has been shown to effectively remove sedative-hypnotics, analgesics and other drugs causing acute intoxication. There is no appreciable clinical toxicity and dramatic shortening of coma time and possible decrease in mortality may be achieved. Thrombocytopenia and clotting may be diminished by pre-perfusion coating with 2.5% albumin. Albumin coating may facilitate the repeated use of hemoperfusion without any complications. More recently, resin hemoperfusion has been used for procainamide, N-acetylprocainamide and theophylline intoxication achieving exceptionally high clearance rates.

Acecainide↗

Anti-histone antibodies in idiopathic and drug-induced lupus recognize distinct intrahistone regions.

We have identified regions within core histones that are antigenic for autoantibodies in systemic lupus erythematosus (SLE) and drug-induced lupus. An immunoblotting technique was used to determine the reactivity of lupus antibodies for intact histones and for trypsin-resistant histone fragments that lack the amino- and carboxyl-terminal amino acids that are normally exposed in native nucleosomes. In SLE, the predominant anti-histone response was restricted to epitopes in the trypsin-sensitive regions. Of 20 SLE sera that had strong antibody activity for multiple intact histones, 17 showed minimal activity with any of the corresponding trypsin-resistant fragments. A markedly different pattern of reactivity was present in sera of patients with procainamide (Pr)-induced lupus in which antibodies to H2A, H2B, and the H2A-H2B complex had strong fragment activity. Interestingly, recognition of trypsin-resistant fragments was also noted in a small number of SLE sera that contained antibodies to the H2A-H2B complex. In contrast to both SLE and Pr-induced lupus, antibodies induced by hydralazine (Hy) reacted primarily with H3 and H4. Furthermore, these antibodies bound equally well to the corresponding trypsin-resistant regions that are thought to be relatively unexposed in native nucleosomes. Thus, the specificities of anti-histone antibodies in SLE, Pr-induced lupus, and Hy-induced lupus are markedly different, but in each disease reactivity appears to be restricted to a limited number of histone determinants. The data raise the possibility that autoantigen in the form of native nucleosomes may be recognized in SLE and possibly in Pr-induced lupus. In contrast, the propensity of Hy to induce autoantibodies to determinants usually not recognized in SLE or Pr-induced lupus may suggest a different immunogenic stimulus in this disease.

Animals↗

Ventricular fibrillation in Wolff-Parkinson-White syndrome, type A.

A young individual who developed ventricular fibrillation following atrial fibrillation in the WPW syndrome is presented. The precise cardiac rhythm diagnosis is extremely important for proper management. When the QRS morphology is bizarre and the ventricular rate is very fast (200 to 300 b.p.m.) in atrial fibrillation, the WPW syndrome should be considered as the underlying disorder. Digitalis should be avoided in this circumstance because anomalous conduction may be accelerated by the drug, leading to deterioration of the clinical picture and even death. When an antiarrhythmic drug is to be used, intravenous lidocaine is the drug of choice. For the prophylactic measure, oral quinidine or procainamide is equally effective for atrial fibrillation with anomalous conduction in the WPW syndrome.

Adult↗

[Protective effects of berberine on spontaneous ventricular fibrillation in dogs after myocardial infarction].

The effects of berberine (Ber 5 mg/kg iv) on ventricular tachyarrhythmias and electrophysiologic consequences in both normal and ischemic myocardium were studied in the open-chest dogs subjected to programmed electrical stimulation (PES) and intimal surface anodal direct current stimulation of the circumflex coronary artery on 5-8 d after acute myocardial infarction. Its effects were compared with procainamide (PA). Both drugs distinctly lengthened the QTc interval and the effective refractory period (ERP) of normal and infarct myocardium in both ventricles and decreased the dispersion of ERP in infarct myocardium (IDR) as well as the dispersion of ERP in left ventricle (VDR). The PES-induced ventricular tachycardia (VT) or ventricular fibrillation (VF) was prevented in 4 out of 6 Ber treated and 5 out of 6 PA treated dogs. Ber prevented spontaneous VF in 4 dogs (n = 5). PA prevented spontaneous VF in 3 dogs (n = 5). Normal saline (NS) did not prevent PES-induced VT/VF and spontaneous VF. The results suggest that Ber may be effective in preventing the onset of reentrant ventricular tachyarrhythmias and sudden coronary death after myocardial ischemic damage.

Animals↗

Phospholipid monolayers and systemic lupus erythematosus.

A hypothesis is presented of the fundamental cause of the systemic lupus erythematosus. From a study of the molecular interaction of procainamide with phospholipid monolayers, it is proposed that the drug causes phospholipid loss from the cell membrane. Chronic phospholipid loss would lead to cell lysis and antinuclear antibody production.

Anesthetics, Local↗

Effect of drugs on the stimulation threshold of the human heart.

Clinical measurements were made of the effects of various drugs on the stimulation threshold of human heart [right ventricle]. Of antiarrhythmic drugs, a marked and prolonged elevation of the stimulation threshold was produced by procainamide, quinidine, and aimaline. Relatively short-lasting elevation was elicited by local anaesthetics [trimecaine, lidocaine]. Beta-blockers were little effective. No detectable effect on the stimulation threshold was produced by phenytoin and digitalis glucosides from the group of antiarrhythmics. The deepest and most prolonged depression of the stimulation threshold was achieved with anabolics [nandrolone phenylpropionate, nandrolone decanoate] and with high doses of prednisone and of 6-methylprednisolone sodium succinate. Hydrocortisone was ineffective. A slight and brief depression was produced by atrophine. The effects of sympathomimetics were complicated: at stimulation with short pulses the threshold was always raised. At stimulation with long pulses the effects were variable, mostly biphasic [occasionally triphasic]: a transitory depression of the stimulation threshold was followed by a marked elevation. The I-t curve's slope altered. In exit block, sympathomimetics are indicated because of their chronotropic effect, not because of their questionable effect on the stimulation threshold. A number of drugs, often administered to stimulated patients, produced no effect on the stimulation threshold: antibiotics, nitrites, purine compounds, opiates, and others.

Adrenergic beta-Antagonists↗

Simultaneous liquid-chromatographic determination of five antiarrhythmic drugs and their major active metabolites in serum.

We report an isocratic "high-performance" liquid chromatographic method for the simultaneous measurement of tocainide, lidocaine, procainamide, quinidine, disopyramide, and their major active metabolites in serum. The drugs are extracted from 200 microL of serum at pH 9.5 with 1.5 mL of 1,2-dichloromethane, concentrated by evaporation, and separated on a CN-bonded-phase column at 40 degrees C (flow rate 2 mL/min) with a pH 7.1 mobile phase of acetonitrile/methanol/phosphate buffer (60/7/33, by vol); the phosphate buffer contains 10 mmol of KH2PO4 and 0.5 mmol of triethylamine per liter. The antiarrhythmic drugs elute in the K' (capacity factor) range of 1.43 (lidocaine) to 5.7 (disopyramide). Results vary linearly with drug concentration to at least 30 mg/L; the detection limit is 0.1-0.2 mg/L. Within-run precision (CV) ranges from 0.9% to 5.0% and day-to-day precision from 2.1% to 6.2%, depending on the specific drug and its concentration in serum. Extraction efficiencies vary from 76% to 85% and analytical recoveries from 98.5% to 103%. At toxic serum concentrations, several basic drugs may interfere with the assay of some antiarrhythmics, but only hydroxyzine, verapamil, and certain local anesthetics interfere at therapeutic concentrations.

Anti-Arrhythmia Agents↗

The effect of buthobendin on glycolysis in rabbit myocardial slices in vitro.

The effect of buthobendin (2S,2'S isomer of N,N'-dimethyl N,N'-bis[1-(3',4',5'-trimethoxybenzoyloxy)-butyl-2]-ethylenediamin e dihydrochloride), (CravitenR) on aerobic and anaerobic glycolysis in rabbit myocardial slices was compared with that of the biologically inactive isomer 2R,2'R and the well-known antiarrhythmic drugs quinidine and procainamide. Only buthobendin stimulated lactate formation under anaerobic and aerobic conditions. However, that effect was not accompanied with a parallel increase in the glucose uptake, but was related to a decrease in the glycogen level. This finding might indicate that buthobendin stimulates glycolysis by mobilization of the glycogen degradation.

Aerobiosis↗

Quantitative toxicology: interlaboratory and intermethod evaluation in New York State.

The New York State Department of Health has conducted a proficiency evaluation program in quantitative toxicology since 1974. Serum samples containing a barbiturate and phenytoin, together with either glutethimide, procainamide, or theophylline, are sent to participating laboratories quarterly. Within the first two years of the program the percentage of laboratories able to quantitate 75% of the test samples to within 25% of the gravimetric values increased from 25 (1974-1975) to 40% (1975-1976). This improvement was partly due to licensure requirements, improved technology for sample preparation and analysis, and the availability of better quality-control practice. An obstacle to obtaining uniform accuracy is the lack of adequate calibration or testing materials. To overcome these obstacles, pure drugs are weighed into a bovine serum matrix, and the weights are confirmed by reference laboratories and used as the target values in the testing program. Comparison of the methods used by participants in this program for barbiturate and phenytoin yielded equations different from those found in other method evaluations.

Barbiturates↗

Use of limited laboratory-acquired therapeutic drug monitoring data in determining individualized drug requirements.

Routinely acquired therapeutic drug monitoring (TDM) data from 220 patients were used to estimate patient-specific pharmacokinetic parameters for the following drugs: aminoglycoside antibiotics (gentamicin and tobramycin), digoxin, theophylline, carbamazepine, procainamide, phenobarbital, and quinidine. A microcomputer based set of algorithms operating on two relatively unconstrained TDM values estimated pharmacokinetic parameters with which future TDM levels were forecast. Mean prediction errors (mpe) and root mean squared errors (rmse) were used as measures of predictive performance. Values of mpe deviated from zero by less than one microgram per l for digoxin and by less than one microgram per l for all other drugs. Values of rmse were also small when viewed in the context of the respective therapeutic plasma concentration ranges.

Adolescent↗

Adverse reactions to antiarrhythmic drugs during therapy for ventricular arrhythmias.

We analyzed the incidence of adverse reactions to antiarrhythmic drugs in 123 consecutive patients with a history of sustained ventricular tachycardia or ventricular fibrillation. Blood levels were measured serially and were maintained within the usual therapeutic range. Minor reactions were defined as those that required dosage reduction and major reactions as those that required drug discontinuation or permanent pacing for bradycardia. A total of 237 individual, oral drug trials were evaluated in the 123 patients. Adverse reactions were noted in 79 trials (33%). Fifty-nine (48%) of the 123 patients had one or more adverse reaction. Major reactions were noted in 36 patients (29%). Adverse effects occurred during 49% of trials with mexiletine hydrochloride, 44% of trials with amiodarone, 24% of trials with procainamide hydrochloride, and 18% of trials with quinidine sulfate or gluconate. In conclusion, clinically significant adverse reactions are common during drug therapy for ventricular arrhythmias. These observations indicate that with the drugs used in this study, an acceptable risk-benefit ratio will be possible only in patients at a significant risk for a symptomatic arrhythmia. Antiarrhythmic drug therapy in patients at low risk for serious arrhythmia should be discouraged.

Aged↗

IgG subclasses of autoantibodies in systemic lupus erythematosus, Sjogren's syndrome, and drug-induced autoimmunity.

The IgG subclasses displayed by autoantibodies were examined in patients with systemic rheumatic diseases. Solid-phase assays performed with purified antigens were combined with a set of four mouse monoclonal antibodies specific for each human subclass to provide quantitative data for all the major autoantibody specificities. IgG1 accounted for an average of 55% of the total antibody activity to native and denatured DNA, Sm antigen, and histone and constituted significantly more anti-SS-B and anti-nRNP (84% and 92%, respectively). The remaining antibody activity consisted largely of IgG3, and this subclass was particularly prominent with anti-histone and anti-Sm in patients with systemic lupus erythematosus. In contrast, IgG2 constituted 3 to 12% of the anti-native and anti-denatured DNA and less than 5% of the anti-SS-B/La activity in only three patients with Sjogren's syndrome. IgG2 was essentially undetectable in antibodies to Sm and RNP antigens. IgG4 was also uncommon, although this isotype was significantly more prevalent in anti-histone from patients treated with procainamide showed that the isotype distribution of anti-histone and anti-denatured DNA remained remarkably constant. However, during periods of large increases in autoantibody activity, a shift from predominantly IgG3 to predominantly IgG1 occurred, consistent with the interpretation that there might be a sequential activation of heavy chain constant regions as the immune response matures. The disproportionately high levels of IgG1 and IgG3 displayed by all the autoantibody specificities examined may indicate that a common immunogenic feature of autoantigens or a common control mechanism underlies the regulation of autoantibody expression.

Antibodies, Monoclonal↗

Butyrylcholinesterase: inhibition by arsenite, fluoride, and other ligands, cooperativity in binding.

Arsenite is a quasi-irreversible inhibitor of human serum butyrylcholinesterase with a dissociation constant of 0.129 mM at pH 7.4, 25 degrees, 0.067 M phosphate, mu = 0.17 M. The inhibition process is second order with a rate constant of 340 M-1 min-1. The first order rate of dissociation, 0.044 min-1, is unaffected by fluoride but is decreased by substrate. The binding of arsenite and fluoride, as determined by the effect of fluoride on the apparent arsenite-enzyme dissociation constant, is highly anticooperative and may be mutually exclusive. The fluoride-enzyme dissociation constant determined from these experiments is 0.90 mM. The binding of a number of other substances, such as dibucaine, is markedly anticooperative with arsenite binding. The binding of some of these substances is positively cooperative with fluoride binding. The effect can be large; procainamide binds 17 times more strongly in the presence of fluoride. Similarly, the mutual binding of benzoylcholine as substrate and fluoride is cooperative, 30-fold, butyrylthiocholine and fluoride, 21-fold, propionylthiocholine and fluoride, 8.3-fold, and acetylthiocholine and fluoride, only 1.8-fold.

Arsenic↗

Atrial flutter in infancy: diagnosis, clinical features, and treatment.

The clinical features and treatment of atrial flutter in eight infants (four male and four female) less than 2 months of age are presented. Atrial flutter was noted during the first week of life in six of the infants and between 6 and 8 weeks of life in the other two infants. Four of the eight infants had associated structural or functional cardiovascular disease, and in three infants a central venous pressure catheter was present in the atrium at the time atrial flutter was diagnosed. Classic flutter waves were apparent on 12-lead ECGs in only two infants. In six infants, flutter waves were not obvious on standard ECGs, but transesophageal electrogram recordings demonstrated the presence of atrial flutter with second degree atrioventricular block. The atrial cycle length during flutter ranged from 135 to 180 ms (mean 149 ms; mean atrial rate 403 beats per minute); there was a 2:1 ventricular response to atrial flutter. Successful termination of atrial flutter was accomplished using three modes of electrical cardioversion in seven of the eight infants: direct current cardioversion in one, transvenous atrial pacing in one, and transesophageal atrial pacing in five. One asymptomatic infant converted to normal sinus rhythm 24 hours following digoxin administration. One infant had multiple atrial flutter recurrences and required chronic procainamide therapy. In seven of the eight infants, no recurrences have been noted in 6 months to 3 1/2 years of follow-up. These results demonstrate that atrial flutter may be difficult to diagnose in infants with tachycardia unless transesophageal electrogram recording is utilized for evaluation.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Flutter↗

Use of serum drug concentrations in outpatient clinics.

A four-month retrospective study was conducted to analyze the use of serum drug concentrations (SDCs) in the outpatient clinics of a teaching hospital. The general internal medicine, asthma and allergy, cardiology, and neurology clinics were selected as frequent users of SDCs. Serum theophylline, digoxin, quinidine, procainamide, carbamazepine, phenytoin, and phenobarbital concentrations obtained during patient clinic visits were audited by trained pharmacy students using medical records and computer-generated laboratory data. The SDCs were evaluated for (1) the appropriateness of how they were obtained, (2) the appropriateness of the actions taken on the results, (3) the reasons they were ordered, and (4) the patient charges secondary to obtaining SDCs incorrectly or taking inappropriate actions on the results. Overall, the SDCs from all the clinics combined were obtained appropriately 251 (61.4%) of 409 times. Appropriate actions were taken on the SDC results 82.4% of the time. A change in therapy was made after an SDC was ordered 24.4% of the time. A total of $4975 of patient charges was associated with incorrectly obtained SDCs or inappropriate actions taken on SDC results. The asthma and allergy clinic, which was staffed by a clinical pharmacist, used SDCs more appropriately than the other clinics. Pharmacists or other professionals should be used to obtain accurate SDC information and to follow-up on SDC results to maximize drug therapy and reduce costs.

Carbamazepine↗

The reversible biotransformation of N-acetylprocainamide in the rhesus monkey.

The specific activity of 14C-N-acetylprocainamide (14C-NAPA) was measured in the 24-h urine of two rhesus monkeys given the labelled drug i.v. Specific activity was found to decrease by 15.8% from the original value. This was attributed to an in vivo biotransformation of NAPA to procainamide (PCA) and reacetylation of PCA back to NAPA before it was eliminated in the urine. The major fraction of NAPA, 72.1% of the dose, was found to be excreted in the urine of monkeys in 48 h.

Animals↗

Serologic abnormalities in spontaneous and drug-induced systemic lupus erythematosus.

Extensive serologic changes occur in systemic lupus erythematosus (SLE) which are probably secondary to unknow primary cause(s). The New Zealand hybrid mouse model most likely has a viral-induced disease and does not show many of the clinical features of the human disease. The best example of human SLE which provides a clue to etiology is the drug-induced type, particularly that due to procainamide. In these patients it is possible to study the development of serologic changes prior to the onset of clinical manifestations, and then observe regression of the clinical and serological changes on withdrawal of the medication. Although there is a rough correlation between the many serologic abnormalities and the clinical picture, enough exceptions exist, so that single tests such as serum complement, anti-DNA antibodies, per cent DNA binding, and others, cannot be used as a sine qua non for management. Care of the patient still remains a clinical problem guided by various laboratory procedures but not dependent on any one. Alkyating agents have a limited role in the treatment of lupus nephropathy and cutaneous vasculitis but azathioprine is probably of no value in SLE.

Animals↗

Inhibition of sulfation of phenols in vivo by 2,6-dichloro-4-nitrophenol: selectivity of its action in relation to other conjugations in the rat in vivo.

The effect of 2,6-dichloro-4-nitrophenol, an inhibitor of the sulfation of the phenolic compound harmol in vivo, on the sulfation of other phenolic substances and on various conjugation reactions has been studied in the rat in vivo. Compounds chemically related to 2,6-dichloro-4-nitrophenol were also tested as sulfation inhibitors. 2,6-Dichloro-4-nitrophenol inhibited the sulfation of phenol while it had no effect on biliary excretion of dibromosulphthalein, glucuronidation of phenolphthalein, acetylation of procainamide ethobromide or glutathione conjugation of ethacrynic acid. It is concluded that of these conjugation reactions sulfation is inhibited selectively at the dose level used. Some phenols with chloro- or nitro-substituents effectively inhibited the sulfation of harmol but to a lesser extent than 2,6-dichloro-4-nitrophenol. Many other phenols did not affect the conjugation of harmol, which is both glucuronidated and sulfated.

Animals↗