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PubMed1990

Bunazosin induces use-dependent slowing of conduction in guinea-pig ventricular myocardium.

The use-dependent effects of bunazosin on the maximal rate of rise (Vmax) of the action potential and conduction velocity were studied in isolated papillary muscles of guinea-pig. Standard microelectrode techniques were used to monitor the conduction and action potential of the muscles. In the presence of 30 microM bunazosin, the time constants for the start of the use-dependent inhibition of Vmax during a 0.2, 1, 2 and 3 Hz stimulation were (means +/- S.E.M. in s) 30.9 +/- 8.0, 15.0 +/- 1.6, 7.4 +/- 0.9 and 3.9 +/- 0.7 (n = 4) and those for conduction velocity were 17.3 +/- 2.3, 17.3 +/- 5.2, 6.5 +/- 0.9 and 3.4 +/- 0.2, respectively. These results showed that in the cardiac ventricular muscle of the guinea-pigs, bunazosin produces use-dependent changes in conduction velocity with onset kinetics comparable to those measured simultaneously using Vmax. The characteristics of the use-dependent inhibition of conduction velocity induced by bunazosin are similar to those found with slow kinetic drugs such as disopyramide rather than with fast ones.

Action Potentials↗

PubMed1995

Effect of lidocaine on alpha 1-adrenoceptors in cultured neonatal rat cardiocytes.

The effect of lidocaine on alpha 1-adrenoceptors in cultured neonatal rat ventricular cardiocytes was studied by binding assay. When the cells were cultured in the presence of lidocaine, the binding of (+/-)-beta-([125I]iodo-4-hydroxyphenyl)-ethyl-aminomethyl-tetralone to the cells increased in a concentration- and time-dependent manner. The effect was due to an increase in maximum binding but not due to a change in the dissociation constant for the ligand. The increased number of alpha 1-adrenoceptors returned to the control level after culturing the cells without lidocaine. The stimulating effect on the number of alpha 1-adrenoceptors of lidocaine was also observed in the presence of norepinephrine. Other class I antiarrhythmic drugs such as procainamide. disopyramide, mexiletine and flecainide increased the number of alpha 1-adrenoceptors in the cells. These results suggest that cardiac responsiveness mediated by alpha 1-adrenoceptors is increased by class I antiarrhythmic drugs.

Adrenergic alpha-Antagonists↗

PubMed1988

Use of cyclic antidepressants in patients with cardiac conduction disturbances.

Cyclic antidepressants can produce cardiac complications in patients with certain types of cardiac conduction abnormalities. Most cyclic antidepressants have a quinidinelike effect on the heart, which, in combination with Type I antiarrhythmic agents such as quinidine, disopyramide and procainamide, may induce heart block and potentially lethal arrhythmias in susceptible individuals. Patients with known cardiovascular disease warrant careful evaluation before tricyclic therapy is initiated. Guidelines are presented for identifying high-risk patients and for using cyclic antidepressants in patients with cardiac conduction abnormalities.

Antidepressive Agents↗

PubMed1984

Susceptibilities of drugs to nitrosation under standardized chemical conditions.

Of 22 drugs with either a N,N-dimethylamino, N,N-diethylamino or N-morpholino group in the molecule, eight were converted to volatile N-nitrosamines by nitrosative cleavage in reactions of nitrite and drug in a molar ratio of 4:1 at pH 3. Under standardized conditions yields were greatest with aminopyrine and minocycline which contains two N,N-dimethylamino groups in the molecule. Oxytetracycline, chlortetracycline, tetracycline, promethazine, chlorpromazine, imipramine and disulfiram gave much lower yields and amitriptyline, clomiphene, clomipramine, dextropropoxyphene, diphenhydramine, disopyramide, erythromycin, mepyramine, methapyrilene, penicillin G procaine salt, procaine, tamoxifen, trimeprazine and tripelennamine yielded no detectable levels of volatile N-nitrosamines. Nitrosation products of 57 drugs were also examined by a group selective procedure estimating both volatile and non-volatile N-nitroso compounds. Virtually all of the yield obtained from aminopyrine or minocycline could be accounted for by N-nitrosodimethylamine (NDMA). However, compounds yielding excess N-nitrosamines compared to NDMA were obtained from the other three tetracyclines, presumably as a result of the cleavage of a methyl group from the N,N-dimethylamino substituent to form desmethyl-N-nitroso compounds. In general, the drugs giving the highest yields of N-nitroso compounds were those containing secondary rather than tertiary amino groups. A considerable range of susceptibilities towards nitrous acid was observed overall; ten drugs containing a secondary or tertiary amino- or amido- or hydrazido - group did not react with nitrous acid to form N-nitroso compounds.

Chemical Phenomena↗

PubMed1993

Relationship between negative inotropic and chronotropic effects of tocainide and five class I antiarrhythmic drugs in the coronary perfused guinea-pig heart.

1. The relationship between the negative inotropic and chronotropic effects of tocainide and 5 other class I antiarrhythmic drugs was evaluated in Langendorff-perfused guinea-pig hearts. 2. All 6 drugs reduced the contractile force (Fc) and the heart rate (HR) of spontaneously beating guinea-pig hearts in a dose-dependent manner. The order of crude negative inotropic potency was: quinidine (Qui) = aprinidine (Apr) > mexiletine (Mex) > lidocaine (Lid) > disopyramide (Dis) > tocainide (Toc); and the order of negative chronotropic effect was: Apr > Qui > Mex > Dis > Lid > Toc. 3. The order of the negative inotropic potency relative to chronotropic effect (expressed as a ratio: ID50 for Fc/ID50 for HR) was Lid > Qui > Dis > Toc > Mex > Apr (n = 6). 4. For heart electrically stimulated at a constant rate, the order of crude negative inotropic potency was: Apr > Qui > Mex > Dis > Lid > Toc, and the order of negative inotropic potency (determined by the ratio: ID50 for Fc in driven heart/ID50 for spontaneously beating HR) was: Mex > Apr > Toc > Dis > Qui > Lid (n = 6). 5. There was a significant influence of negative chronotropic effect on the inotropic potency and the order was: Lid > Qui > Dis > Toc > Apr > Mex. The potency of various drugs is clinically useful in the choice of drugs when considering cardiac function and heart rate.

Animals↗

PubMed1993

High-performance liquid chromatographic method for the simultaneous determination of pentisomide and its major metabolite N-desisopropylpentisomide in plasma, urine and tissues using solid-phase extraction.

A rapid, sensitive and selective high-performance liquid chromatographic method for the simultaneous determination of pentisomide and its major metabolite desisopropylpentisomide in plasma, urine and tissues has been developed. The method for plasma samples, urine samples and tissue samples, after homogenizing with 50% ethanol, involves extraction of samples via activated Bond-Elut C8 disposable columns with methanol at pH 10 after addition of internal standard, and initially on column washing of samples at pH 10 with water and acetonitrile. The obtained methanolic extract is evaporated to dryness under nitrogen at 25 degrees C; the sample residue is then reconstituted in mobile phase and an aliquot of this solution is injected into the liquid chromatograph. Separation is performed using a Nova-Pak C18 4 microns particle size column operating in combination with radial compression separation unit and a methanol-water-di-sec.-butylamine-phosphoric acid (40:60:0.5:0.2, v/v) pH 3.5 mobile phase with ultraviolet detection at 258 nm. Endogenous substances or a variety of drugs concomitantly used in pentisomide therapy, with the exception of disopyramide, do not interfere with the assay. The mean recovery of pentisomide and desisopropylpentisomide from plasma and urine and from tissues is more than 91 and 86%, respectively. The limit of detection of the assay is 10 ng/ml for both drugs. The intra- and inter-day coefficient of variation for replicate analyses of spiked plasma samples is less than 7 and 8%, respectively. Mean steady-state plasma levels of pentisomide and desisopropylpentisomide in patients on chronic oral therapy are reported.

Anti-Arrhythmia Agents↗

PubMed1994

Use of sertraline hydrochloride in the treatment of refractory neurocardiogenic syncope in children and adolescents.

OBJECTIVES: The purpose of our study was to determine whether the serotonin reuptake inhibitor sertraline hydrochloride could prevent neurocardiogenic syncope in children and adolescents resistant to or intolerant of other therapies. BACKGROUND: The serotonin reuptake inhibitor fluoxetine hydrochloride has been reported to be effective in preventing neurocardiogenic syncope in adults. METHODS: Seventeen consecutive young patients (mean age 15 years, range 10 to 18; 7 male, 10 female) with recurrent syncope and a positive head-upright tilt table test, and in whom standard therapies (fludrocortisone, transdermal scopolamine, beta-adrenergic blocking agents, disopyramide) were ineffectual, poorly tolerated or contraindicated, were referred for study. Sertraline was administered orally at 50 mg daily for 4 to 6 weeks. A head-upright tilt table test was then reperformed, and the clinical effect was noted. RESULTS: Three patients (18%, 95% confidence interval [CI] 1 to 44) were intolerant of the drug, and it was discontinued. Nine patients became asymptomatic and tilt negative (53%, 95% CI 26 to 76), and five remained tilt positive (36%, 95% CI 15 to 65). Over a mean follow-up period of 12 +/- 5 months, the tilt-negative patients remained symptom free while taking sertraline. CONCLUSIONS: The serotonin reuptake inhibitor sertraline hydrochloride can be effective in preventing recurrent neurocardiogenic syncope in selected patients unresponsive to or intolerant of other therapeutic modalities.

1-Naphthylamine↗

PubMed2026

Microglial PICALM: A novel genetic driver and therapeutic target in vascular dementia.

BACKGROUND: Vascular dementia (VaD) lacks well-defined genetic mechanisms. Cell-type-specific effects of GWAS loci remain unexplored. METHODS: We integrated single‑cell eQTL data (183 donors, eight cell types) with VaD GWAS (3624 cases, 475,484 controls) using Mendelian randomization and Bayesian colocalization, replicated in an independent cohort (2074 cases, 456,366 controls). Subtype, snRNA‑seq, cell‑cell communication, PheWAS, expression profiling, and drug prediction with BBB permeability assessment were performed. RESULTS: Microglial PICALM was the only robustly replicated signal (OR = 0.8334, p = 5.3 × 10⁻⁴; colocalization PP.H4 > 0.75). The effect was strongest in multiple infarctions dementia (OR = 0.7746). Exploratory snRNA-seq analysis (4 VaD vs. 4 controls; GSE282111) provided supporting evidence for microglial PICALM enrichment and downregulation (p < 0.001). PICALM‑high microglia showed enhanced neurovascular‑ and phagocytosis‑related communication (e.g., SPP1, GAS6, GRN). PheWAS revealed no pleiotropy. In silico drug repurposing prioritised three FDA-approved BBB-penetrant compounds (disopyramide, benzocaine, amantadine) as candidates warranting further mechanistic validation. CONCLUSIONS: Microglial PICALM is identified as a likely genetic determinant of VaD, especially in the multiple infarctions subtype. Upregulating PICALM may be associated with a neuroprotective microglial phenotype, highlighting PICALM as a candidate therapeutic target warranting further experimental validation.

Humans↗

PubMed2004

Accuracy of calculated pH-dependent aqueous drug solubility.

The aim of the present study was to investigate the extent to which the Henderson-Hasselbalch (HH) relationship can be used to predict the pH-dependent aqueous solubility of cationic drugs. The pH-dependent solubility for 25 amines, carrying a single positive charge, was determined with a small-scale shake flask method. Each sample was prepared as a suspension in 150 mM phosphate buffer. The pH-dependent solubility curves were obtained using at least 10 different pH values. The intrinsic solubility, the solubility at the pKa and the solubility at pH values reflecting the pH of the bulk and acid microclimate in the human small intestine (pH 7.4 and 6.5, respectively) were determined for all compounds. The experimental study revealed a large diversity in slope, from -0.5 (celiprolol) to -8.6 (hydralazine) in the linear pH-dependent solubility interval, which is in sharp contrast to the slope of -1 assumed by the HH equation. In addition, a large variation in the range of solubility between the completely uncharged and completely charged drug species was observed. The range for disopyramide was only 1.1 log units, whereas that for amiodarone was greater than 6.3 log units, pointing at the compound specific response to counter-ion effects. In conclusion, the investigated cationic drugs displayed compound specific pH-dependent solubility profiles, indicating that that the HH equation in many cases will only give rough estimations of the pH-dependent solubility of drugs in divalent buffer systems.

Hydrogen-Ion Concentration↗

PubMed2004

Acute ventricular rate control in atrial fibrillation and atrial flutter.

Atrioventricular node blocking agents including beta-adrenergic blockers, non-dihydropyridine calcium channel blockers and digoxin are usually effective in controlling ventricular rate in atrial fibrillation and flutter. Intravenous beta-blockers and non-dihydropyridine calcium channel blockers are equally effective in rapidly controlling the ventricular rate. The addition of digoxin to the regimen causes a favorable outcome but digoxin as a single agent is generally less effective in slowing the ventricular rate in acute setting. Clonidine, magnesium, and amiodarone have also been used for acute ventricular rate control in atrial fibrillation. Limited data suggest that combination regimens provide better ventricular rate control than any agent alone. The agent of first choice is usually individualized depending upon the clinical situation. Beta-blockers are preferable in patients with myocardial ischemia, myocardial infarction and hyperthyroidism and in post-operative state, but should be avoided in patients with bronchial asthma and chronic obstructive pulmonary disease where non-dihydropyridine calcium channel blockers are preferred. Beta-blockers are preferred drugs used for acute ventricular rate control in atrial fibrillation during pregnancy. In atrial fibrillation with Wolff-Parkinson-White syndrome, beta-blockers, calcium channel blockers and digoxin should be avoided, as these drugs are selective atrioventricular node blockers without slowing conduction through the accessory pathway, which can lead to increased transmission of impulses preferentially through the accessory pathway and precipitate ventricular fibrillation. The drug of choice for atrial fibrillation in pre-excitation syndrome is procainamide but propafenone, flecainide and disopyramide have also been used. When clinical condition is unstable or patient is hemodynamically compromised, immediate electrical cardioversion is the treatment of choice, as the best measure to control ventricular rate is by conversion to sinus rhythm. Factors precipitating rapid ventricular rate should be treated as well.

Atrial Fibrillation↗

PubMed1990

Barucainide, a novel class Ib antiarrhythmic agent with a slow kinetic property: electrophysiologic observations in isolated canine and rabbit cardiac muscle.

Electrophysiologic effects of barucainide hydrochloride on the transmembrane potentials of isolated canine and rabbit cardiac muscle were investigated by means of a standard microelectrode technique. Barucainide (10(-6) to 3.0 x 10(-5) mol/L) produced concentration-dependent inhibition of the maximum upstroke velocity (Vmax) in canine Purkinje fibers and ventricular muscle. Tonic block of Vmax was small and negligible. Barucainide produced marked use-dependent block (UDB). The onset rate of UDB and the speed of recovery from UDB were comparable to those of disopyramide. The recovery time constant was 8.0 +/- 0.8 seconds. Membrane depolarization induced by high concentrations of potassium enhanced the inhibitory action of barucainide on Vmax. The enhancement of tonic block was much greater than that of UDB indicating a selective effectiveness of the drug in pathologically depolarized tissues. Barucainide produced marked shortening of the action potential duration (APD), which indicates that barucainide exerts class Ib antiarrhythmic effects. Such shortening effects on the APD were not affected by pretreatment with 1 mmol/L cobalt or with 0.5 mmol/L 4-aminopyridine. In contrast, barucainide had no marked effects on the APD in the presence of 4.0 x 10(-5) mol/L lidocaine, although it produced almost the same extent of Vmax inhibition as did barucainide alone. Frequency of the pacemaker activity in the rabbit sinoatrial tissue and of the automaticity at normal resting potential in Purkinje fibers enhanced by 2.0 X 10(-6) mol/L isoproterenol were significantly suppressed by barucainide. However, barucainide up to 3.0 x 10(-5) mol/L failed to suppress the firing frequency of the abnormal automaticity in canine Purkinje fibers induced by 5 mmol/L barium. These overall findings indicate that barucainide is a novel class Ib antiarrhythmic agent which, unlike other Ib agents, has a slow kinetic property. However, the precise significance of this unique electrophysiologic feature with respect to the antiarrhythmic action of the drug is not known but provides the basis for understanding the relationship of electrophysiologic effects of barucainide in vitro and its potential antiarrhythmic actions in experimental animals and in humans.

4-Aminopyridine↗

PubMed1998

Drug treatment of atrial fibrillation in the managed care era.

There are many reasons why one might wish to suppress atrial fibrillation (AFib) and attempt to maintain sinus rhythm. This article assumes that the clinical decision to maintain sinus rhythm has been made. That being the case, antiarrhythmic drug therapy is generally the first line of treatment of AFib. Currently in the United States, there are 8 available antiarrhythmic drugs that have demonstrated efficacy for preventing AFib. The drugs are quinidine, procainamide, disopyramide, flecainide, propafenone, moricizine, sotalol, and amiodarone. Because AFib tends to recur regardless of the drug selected, recurring in at least one-half of the patients being treated, no drug is clearly better than any other for suppression of AFib. Furthermore, because AFib is rarely life-threatening, occasional recurrence should be anticipated and should not be considered failure per se. The measure of drug efficacy is the frequency of recurrence. Before initiating drug therapy, the presence or absence of structural heart disease must be determined, because in the absence of structural heart disease, antiarrhythmic drugs generally can be given rather safely, but in the presence of structural heart disease, especially when associated with ventricular dysfunction, there is an important risk of developing ventricular proarrhythmia. Considerations for specific drug selection are discussed and an algorithm for therapy is suggested.

Anti-Arrhythmia Agents↗

PubMed1999

Enhancing effects of salicylate on tonic and phasic block of Na+ channels by class 1 antiarrhythmic agents in the ventricular myocytes and the guinea pig papillary muscle.

OBJECTIVE: To study the interaction between salicylate and class 1 antiarrhythmic agents. METHODS: The effects of salicylate on class 1 antiarrhythmic agent-induced tonic and phasic block of the Na+ current (INa) of ventricular myocytes and the upstroke velocity of the action potential (Vmax) of papillary muscles were examined by both the patch clamp technique and conventional microelectrode techniques. RESULTS: Salicylate enhanced quinidine-induced tonic and phasic block of INa at a holding potential of -100 mV but not at a holding potential of -140 mV; this enhancement was accompanied by a shift of the hinfinity curve in the presence of quinidine in a further hyperpolarized direction, although salicylate alone did not affect INa. Salicylate enhanced the tonic and phasic block of Vmax induced by quinidine, aprindine and disopyramide but had little effect on that induced by procainamide or mexiletine; the enhancing effects were related to the liposolubility of the drugs. CONCLUSIONS: Salicylate enhanced tonic and phasic block of Na+ channels induced by class 1 highly liposoluble antiarrhythmic agents. Based on the modulated receptor hypothesis, it is probable that this enhancement was mediated by an increase in the affinity of Na+ channel blockers with high lipid solubility to the inactivated state channels.

Action Potentials↗

PubMed1983

Effect of antiarrhythmic drugs on serum free fatty acid levels during experimental cardiac arrhythmias in the cat.

The level of free fatty acid (FFA) in serum has been estimated before and after ventricular fibrillation (VF) induced by electrical stimulation, intravenous administration of ouabain, aconitine or ligation of the left anterior descending branch of coronary artery. FFA contents were found to be significantly increased after VF. Quinidine, disopyramide, lidocaine and phenoxybenzamine, when administered intravenously 30 min before electrical stimulation (E.S.), have no effect on serum FFA contents by themselves. All the antiarrhythmic drugs except phenoxybenzamine prevent the rise in FFA contents normally observed after VF. These drugs in appropriate doses also protect the animals against VF upto 100 volts. Propranolol did not provide protection against VF but prevented increase in FFA levels. Verapamil neither showed any protection against VF nor blocked the elevation of FFA after E.S. These results indicate that most of the antiarrhythmic drugs which are effective against the precipitation of VF by E.S. block the increase in serum FFA levels.

Animals↗

PubMedDate not supplied

Management of patients with life-threatening sustained ventricular tachyarrhythmias--the role of guided antiarrhythmic drug therapy.

Two recent studies have evaluated the utility of electrophysiologic (EP) testing in the treatment of patients with serious ventricular arrhythmias. The first study compared electrophysiologically guided antiarrhythmic drug therapy with nonguided beta-blocker therapy. Patients without inducible arrhythmias were assigned to oral metoprolol; patients with inducible arrhythmias were randomly assigned to receive either oral metoprolol or EP-guided drug therapy with propafenone, flecainide, disopyramide, sotalol, or amiodarone. Antiarrhythmic drugs were tested in a random order, but amiodarone was always tested last. A total of 170 patients were evaluated; 115 patients had inducible arrhythmias, and 61 patients were randomly assigned to serial drug testing, 54 to metoprolol without invasive testing, and the remainder who were noninducible to empiric metoprolol. The best outcome was observed in patients without inducible arrhythmias, all of whom received metoprolol. There was no difference in outcome between the two groups with inducible arrhythmias, either treated with metoprolol or with EP-guided serial antiarrhythmic drug testing. The second study evaluated survivors of out-of-hospital ventricular fibrillation (VF) without new myocardial infarction. Patients received assessment of left ventricular ejection fraction, Holter monitoring (HM), and EP testing. Only patients with inducible sustained ventricular arrhythmias or with sufficient ambulatory ventricular ectopy were included in the study. Therapy was randomized either to empiric amiodarone or conventional drug therapy guided by EP testing and/or HM. A total of 228 patients were treated, 113 with amiodarone and 115 with conventional antiarrhythmic drug therapy. The composite primary end points were total mortality, documented out-of-hospital resuscitation from recurrent VF, or syncopal implantable cardioverter/defibrillator shock followed by return of consciousness. Patients treated with empiric amiodarone had a better outcome than did patients treated with guided conventional drug therapy. In those patients in whom an implantable cardioverter/defibrillator was used, patients treated with amiodarone had fewer total shocks and fewer syncopal shocks than did patients treated with conventional therapy. Patients with a history of out-of-hospital VF or sustained ventricular tachycardia without inducible ventricular arrhythmias at EP study have the best outcome. Empiric metoprolol is equivalent to conventional antiarrhythmic drug therapy guided by EP testing. Empiric amiodarone is superior to conventional antiarrhythmic drug therapy guided by HM and/or EP testing.

Adrenergic beta-Antagonists↗

PubMed1996

Inhibition of synaptosomal veratridine-induced sodium influx by antidepressants and neuroleptics used in chronic pain.

Veratridine-induced (10 microM) increases in intracellular sodium ([Na+]int) or calcium ([Ca2+]int) in rat cortical synaptosomes, measured with the fluorescent dyes SBFI or FLUO-3 were blocked by tetrodotoxin (IC50 Na+ 14 nM; Ca2+ 20 nM) and by a series of reference sodium channel blockers with neuroprotective (riluzole, lifarizine IC50 approximately 1-5 microM), anticonvulsant (lamotrigine, phenytoin IC50 approximately 70-140 micro M), local anaesthetic (lidocaine, procaine IC50 approximately 60-200 microM) or antiarrhythmic properties (quinidine, disopyramide, amiodarone, mexiletene, propafenone, fleicainide IC50, approximately 2-200 microM). Potencies for inhibition of veratridine-induced sodium and calcium entry were closely matched. These agents did not, or only weakly blocked, potassium evoked (50 mM) increases in [Ca2+]int. A number of antidepressant monoamine uptake inhibitors (amitriptyline, fluoxetine, clomipramine, desipramine, imipramine) or neuroleptics (pimozide, cinnarizine, haloperidol) were also potent inhibitors of veratridine-induced increases in [Na+]int or [Ca2+]int with affinities ranging from approximately 1-10 microM. A number of these drugs, from diverse chemical and pharmacological classes, are used for the treatment of chronic pain and their mechanism of action could perhaps be related to their common effects on a particular species of neuronal sodium channel.

Analgesics↗

PubMed1986

Determination of pindolol in human plasma and urine by high-performance liquid chromatography with ultraviolet detection.

This paper presents a rapid, simple and economical method for assaying pindolol concentrations in plasma and urine by high-performance liquid chromatography using ultraviolet detection. It is sensitive enough for use in single-dose pharmacokinetic studies and may also be used to determine pindolol concentrations in the plasma from patients taking the drug, provided that the patient is not taking any of the drugs which interfere with the method. Drugs which were found to interfere with the pindolol peak are quinidine, n-acetylprocainamide and lidocaine. Disopyramide, oxprenolol and levobunolol interfered with the internal standard peak.

Alprenolol↗

PubMed2002

Quantification of pilsicainide in serum by capillary electrophoresis.

A new method for determining pilsicainide concentration in serum by rapid and selective capillary electrophoresis has been developed and validated. For pretreatment, serum was made alkaline and then extracted with diethyl ether. Procainamide was used as an internal standard. Sodium dihydrogenphosphate buffer (pH 2.29; 0.1 M) was used as a running buffer. A fused-silica capillary tube was loaded with a voltage of 25 kV and detection was performed at UV 200 nm. Good linearity (0-2.5 microg/ml) was obtained with the minimum limit of detection being 0.04 microg/ml serum (signal-to-noise ratio, 3:1). The R.S.D. of within-run reproducibility was 0.798-2.32%, that of between-run reproducibility was 4.74-5.12% and the recovery rate was 61-63%. Disopyramide, another anti-arrhythmic drug, was close to pilsicainide in terms of migration time. This method was applied to determination of pilsicainide in serum samples.

Anti-Arrhythmia Agents↗