Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: CAS:41708-72-9 (Tocainide)
 93 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tinnitus is the subjective perception of sound that does not exist. Tinnitus is caused by an altered discharge in the auditory pathway from hair cell to cortex and back. Intravenous Xylocaine acts by blocking 10% of the transmission through each synapse, having more effect on the slow multisynaptic pathway through the reticular formation than the rapid pathway to have more effect on the low frequency slow pathway tinnitus than the rapid pathway high frequency tinnitus. Tocainide, the oral amide of Xylocaine, is of great value in the treatment of tinnitus responsive to intravenous Xylocaine.
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PMID:Medical treatment of tinnitus. 392 54

Tocainide, a newly released class 1B antiarrhythmic agent, has membrane stabilizing and electrophysiologic characteristics similar to those of lidocaine, but it can be prescribed for oral administration. Investigational studies in both animals and humans have shown tocainide's effectiveness for the treatment of ventricular arrhythmias in chronic and acute settings. The drug has nearly 100% bioavailability after oral administration and an effective half-life of 9 to 37 hours (mean, 15 hours). Antiarrhythmic efficacy is similar to that of other class I medications currently in use. Serious side effects most frequently involve the central nervous or gastrointestinal system and occur in 10% to 20% of patients. Tocainide has minimal negative inotropic effects and a tendency to shorten effective refractory periods.
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PMID:Tocainide: a new oral antiarrhythmic agent. 392 7

Tocainide (W-36095, Xylotocan) is a derivative of lidocaine which is applied clinically as a cardiac antiarrhythmic. In addition, it diminishes the severity of symptoms in neurological disorders such as myotonia and paramyotonia and in patients with torticollis spasmodicus it brings about a distinct reduction in the tension of the neck muscles. It was investigated whether in reducing the tonus in torticollis spasmodicus tocainide could be acting on the central nervous system. The binding affinity of the substance to the dopamine, serotonin, opiate, GABA and benzodiazepine receptors was measured without finding any significant affinities. In addition, the effect of tocainide on the concentration of the neurotransmitters norepinephrine (noradrenaline), dopamine, serotonin and histamine were investigated in rat brain, and it was found that tocainide induces a significant increase in dopamine and serotonin concentrations. This lead to the conclusion that, in addition to its antiarrhythmic effects, tocainide acts on the central nervous system.
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PMID:Effect of tocainide on the concentrations of norepinephrine dopamine, serotonin and histamine in rat brain and its binding affinity to neuroceptors. 392 26

Tocainide is an orally active lidocaine analog indicated for the suppression of ventricular arrhythmias. It is electrophysiologically similar to lidocaine and produces minimal hemodynamic and electrocardiographic changes. Oral bioavailability is virtually complete, elimination half-life is 11-15 hours, and 40 percent of a dose is excreted unchanged in urine. Tocainide therapy is commonly associated with gastrointestinal and neurologic side effects that generally are well tolerated. Rash, aggravation of arrhythmias, and worsening of heart failure may also occur. While tocainide does not consistently suppress arrhythmias following myocardial infarction, it does control chronic ventricular arrhythmias, being particularly effective in patients responsive to lidocaine. Tocainide has not been shown to be more effective than quinidine or procainamide. Tocainide should be a useful agent in patients who are unable to tolerate other antiarrhythmics, who are responsive to lidocaine, or who have been troubled with Q-T prolongation with or without torsade de pointes.
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PMID:Tocainide: a new oral antiarrhythmic. 392 8

Comparison of the action of tocainide in guinea pig atrial and ventricular myocardium has led to the following results: Tocainide effects a similar increase in threshold of alternating current induced arrhythmias in spontaneously beating right atria as well as stimulated left atria and papillary muscles. APD30 and APD90 (action potential duration at 30 and 90% repolarization) are decreased by tocainide in papillary muscles, especially at a low stimulation rate, but increased in left atria. On the other hand, maximum upstroke velocity of the action potential (Vmax) is decreased at a high stimulation rate (use-dependence) in both tissues. These effects are completely reversed by washing with drug-free solution within 15 min in papillary muscles and 60 min in left atria, respectively. Resting state block of Na-channels by tocainide occurs in left atria to a small degree (10-20%), but is negligible in ventricular myocardium. Recovery of Vmax following stimulus-induced inactivation is delayed by tocainide in papillary muscles and left atria. Functional refractory period is increased in left atria and in papillary muscles by tocainide. In the concentration range above 75 mumol/l the concentration response curve reaches a plateau in papillary muscles but shows a further steep increase in left atria. Quantitative analysis of the dynamic Na-channel blockade by tocainide in atrial myocardium using the modulated receptor hypothesis suggests that the drug shows a high affinity to activated and a low affinity to inactivated Na-channels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrophysiological and antiarrhythmic actions of tocainide in isolated heart preparations of the guinea pig. 393 6

The administration of beta-receptor blocking drugs and antiarrhythmic drugs in close proximity may result in hemodynamic, electrophysiologic, or pharmacokinetic interactions. We examined the hemodynamic and electrophysiologic effects of 0.20 mg/kg intravenous metoprolol followed by a 15-minute infusion of 0.75 mg/kg/min tocainide. In the six patients sutided, metoprolol produced a fall in cardiac rate and output which was not further altered by tocainide. Both drugs decreased peak left ventricular (LV) dP/dt, ejection fraction, and mean Vcf. There was no change in LV end-diastolic pressure or echo dimension and in clinical ill effects. In eight patients without sinus A-V nodal disease electrophysiologic studies showed mild depression of A-V conduction by metoprolol. Tocainide depressed sinus node function and shortened the functional refractory period of the His-Purkinje system. There were no clinical sequelae. However, three patients with preexisting electrophysiologic abnormalities developed asystole. There was no evidence of pharmacokinetic interaction. It is concluded that metoprolol and tocainide can be given concurrently with reasonable safety to cardiac patients without electrophysiologic abnormalities.
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PMID:Hemodynamic and electrophysiologic interactions between antiarrhythmic drugs and beta blockers, with special reference to tocainide. 610 7

Recent studies have shown that the sodium conductance of the sarcolemma is disturbed in paramyotonia. Tocainide is a new antiarrhythmic agent which seems to reduce effectively sodium conductance. Eight patients with paramyotonia were treated with tocainide, whereby the paramyotonic stiffness and weakness brought about by cooling could be prevented.
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PMID:Successuful treatment of paramyotonia congenita (Eulenburg): muscle stiffness and weakness prevented by tocainide. 624 9

Tocainide, an oral analog of lidocaine, was evaluated as a long-term antiarrhythmic agent in 21 patients with symptomatic complex ventricular ectopic activity (10 with hemodynamically significant ventricular tachycardia) refractory to currently available antiarrhythmics singly, and in combination for periods of 3 days to 35 months (mean 13.6 months). Tocainide appeared to be an effective and safe agent for the control of these refractory symptomatic ventricular arrhythmias in 14 of the 21 patients (66%). Minor central nervous system and gastrointestinal side effects were present in most of the patients, usually early on in therapy, and only precluded long-term use in 2 patients. Furthermore, lidocaine responsiveness was a good predictor of tocainide effectiveness in this group of patients. Tocainide precipitated atrioventricular (A-V) block in one patient with pre-existing A-V nodal disease; two patients developed a skin rash while on tocainide therapy. These two patients had previously developed lupus-like syndromes and skin rashes while on procainamide. The ANA titers had been falling in these two patients while on tocainide, and in one of these patients with true systemic lupus erythematosus, rechallenge with tocainide failed to produce skin rash. Tocainide's long plasma half-life and high oral bioavailability permit an 8-h regime. We conclude that tocainide is an effective, safe antiarrhythmic agent with tolerable side effects.
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PMID:Chronic tocainide therapy for refractory high-grade ventricular arrhythmias. 640 67

Tocainide is a new antiarrhythmic agent that is used clinically as the racemic mixture. In order to study the disposition of the individual enantiomers in man, a gas--liquid chromatographic assay was developed based on the resolution of the R-(-)- and S-(+)-enantiomers as their heptafluorobutyryl derivatives on a capillary column coated with a chiral stationary phase. Two healthy male volunteers ingested an oral solution dose of racemic tocainide hydrochloride at a dose of 3 mg/kg and plasma and urine were collected at intervals for up to 54 h. Analysis of the plasma samples revealed a stereoselective disappearance of the R-(-)-enantiomer, such that the apparent half-life for the S-(+)- and R-(-)-enantiomers were 25.6 and 20.5 h, respectively in one subject and 11.1 and 9.0 h in the second subject. Similar relationships were observed in urine, where the ratio of the S-(+)- to R-(-)-enantiomers varied from 0.98 in 1 h to 3.03 in the 54-h samples in one subject over the same time period.
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PMID:Gas--liquid chromatographic resolution and assay of tocainide enantiomers using a chiral capillary column and study of their selective disposition in man. 640 13

In this paper some of the new antiarrhythmic drugs are reviewed. The origin, electrophysiologic effects, mechanisms of action, pharmacokinetic properties, hemodynamic changes, clinical utilization with indications and contraindications as well as the collateral effects of: Verapamil Amiodarone, Aprindine, Encainide, Mexiletine and Tocainide are analyzed. A conclusion is drawn for each one of these drugs in accordance with the available information in the literature and the author's criteria and experience.
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PMID:[New anti-arrhythmia drugs]. 641 Oct 15


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