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PubMedDate not supplied

Relative electrophysiological potencies of quinidine, 3-OH quinidine and quinidine-N-oxide in guinea-pig heart.

The relative potencies of the quinidine metabolites, 3-OH quinidine (3OHQ) and quinidine-N-oxide (QNO), to their parent drug, quinidine, were obtained electrophysiologically using guinea-pig hearts. The items examined were QT interval of local extracellular electrogram in a Langendorff's perfused heart, effective refractory period (ERP) and action potential duration at 90% repolarization (APD90) in the right papillary muscle. Quinidine (0.125-1 mg/l) and 3OHQ (0.5-4 mg/l) prolonged QT interval in a concentration-dependent manner and the relative potency of 3OHQ to quinidine was 0.25. The effect of QNO on QT interval within the range of concentration used (up to 8 mg/l) was small and the relative potency was 0.04 at the most. An apparent additive effect of 3OHQ to that of quinidine was revealed, but QNO of 4 mg/l has no effect on the concentration-effect relationship of quinidine for prolonging QT interval. These results were quite similar to those in humans reported previously. Quinidine (0.5-4 mg/l), 3OHQ (1-8 mg/l) and QNO (2-8 mg/l) prolonged APD90 in a concentration-dependent manner. These effects were accompanied by the prolongation of ERP in similar degrees. The relative potencies of 3OHQ to Q were 0.22 for APD90 and 0.27 for ERP and those of QNO were 0.087 for APD90 and 0.084 for ERP. Quinidine (10(-5) M) depressed the maximum upstroke of action potential (Vmax) in a frequency-dependent manner. 3OHQ of the same concentration also depressed it in the same manner to a much lesser extent and QNO had no effect. In conclusion, relative potencies of quinidine metabolites to quinidine for prolonging QT interval of local extracellular electrogram represent those to prolong APD90 and ERP, suggesting the relative potencies for antiarrhythmic activity in the same order. In the physiological range of concentrations of metabolites, 3OHQ may contribute to the antiarrhythmic effect of quinidine in an additive way, but QNO may have little effect when we take into account the fact that the free fraction of 3OHQ is 2.5 times that of quinidine.

Action Potentials↗

PubMed1983

Steady-state bioavailability of two sustained-release quinidine preparations: quinidine gluconate versus quinidine sulfate.

Steady-state bioavailability of a sustained-release quinidine gluconate formulation was compared with that of a sustained-release quinidine sulfate preparation in a crossover study. Sixteen healthy men were given multiple doses (two tablets every 12 hours) of the two drugs in randomized sequence. Blood samples were obtained immediately before administration of the seventh dose (hour 70) and at 1, 2, 3, 4, 5, 6, 8, 10, and 12 hours after administration. Plasma samples were assayed for quinidine content by high-performance liquid chromatography, with the analyst unaware of the identity of the drug in the sample. On a tablet-for-tablet basis, the sustained-release quinidine gluconate tablets achieved significantly higher plasma levels between two and six hours, higher mean area under the curve, and higher mean maximum concentrations than did the sustained-release quinidine sulfate tablets. When the data were adjusted to correct for the 23% higher quinidine content in the quinidine sulfate tablets, plasma levels from the sustained-release quinidine gluconate were significantly higher than those from quinidine sulfate at all sampling points. Moreover, the sustained-release quinidine gluconate provided significantly greater bioavailability as determined by all pharmacokinetic parameters. Steady-state pharmacokinetics of sustained-release quinidine products cannot be predicted from single-dose studies. The present multiple-dose study demonstrated that, under steady-state conditions, sustained-release quinidine gluconate tablets are more available systemically than sustained-release quinidine sulfate tablets.

Biological Availability↗

PubMedDate not supplied

Urinary excretion kinetics of intact quinidine and 3-OH-quinidine after oral administration of a single oral dose of quinidine gluconate in the fasting and non-fasting state.

To obtain more precise urinary excretion data of intact quinidine (D) and its main metabolite, 3-OH-quinidine (DM), the specific HPLC method of Bonora et al has been used to follow its urinary excretion kinetics. In a cross-over study, 2 commercial dosage forms of quinidine gluconate, fast- and slow-release, were administered to 18 healthy subjects who had fasted for 10 hours in 3 treatments which were administered during the fasting period (T1), and before (T2) of after (T3) a standard breakfast. The urine was collected at fixed time intervals for 72 hours after the administration of a single dose (405 mg of quinidine base). The difference between the drug release characteristics of the two products was studied by analysing the cumulative amount of D and DM excreted as a function of time, and the time required to reach the maximum value for the urinary excretion rate of intact quinidine. A food effect could be noticed among treatments with the conventional fast-release dosage form when comparing the maximum values of the urinary excretion rate of D (T2 greater than T1). There was no significant difference in the percentage of drug absorbed from the 2 products, according to the data on the cumulative amount of D and DM. The parameters estimated for quinidine and the metabolite were: the apparent half-life of elimination, the urinary excretion rates and the time to reach a maximum value in the urinary excretion rate. The urinary excretion rate constant and the renal clearance were also quantified for quinidine by combining urinary parameters with the corresponding serum data previously reported.

Administration, Oral↗

PubMedDate not supplied

Application of 1H-nuclear magnetic resonance spectroscopic method for quinidine to simultaneous determination of quinidine and dihydroquinidine in quinidine sulfate tablets.

Based on the structural differences between quinidine and dihydroquinidine, a 1H-nuclear magnetic resonance spectroscopic method previously reported for quinidine drug substance was modified and shown to be applicable to the quantitative determination of both compounds in quinidine sulfate tablets. Deuterated chloroform was used as the solvent and hexamethylcyclotrisiloxane served as an internal standard. The average recovery and standard deviation of quinidine sulfate (calculated as the sum of quinidine sulfate plus dihydroquinidine sulfate) from synthetic formulations was 98.94 +/- 0.43% (n = 10). Five lots of 200 mg tablets of quinidine sulfate from one commercial source were found to contain from 92.9 to 95.8% quinidine sulfate, and from 1.1 to 7.0% dihydroquinidine sulfate.

Magnetic Resonance Spectroscopy↗

PubMedDate not supplied

Comparative quinidine plasma profiles at steady state of two controlled-release products and quinidine sulfate in solution.

A study was conducted to compare, at steady state, the plasma quinidine level profiles of two commercial controlled-release products (quinidine sulfate controlled release and quinidine gluconate controlled release) with quinidine sulfate given in solution. Twenty-four healthy volunteers entered the study and 23 completed it. Quinidine formulations were given at 600 mg day-1 for 4 days in each of three periods in a randomized crossover study. In addition to frequent blood sampling on the fourth day of each period, samples were taken during the approach to steady state to confirm by minimum plasma concentrations (Cmin) that steady state had been attained. Quinidine concentrations were measured by using a high-performance liquid chromatographic assay specific for quinidine. The bioavailability of the two controlled-release products relative to quinidine sulfate in solution was adequate when dose correction to account for differences in quinidine base content was done. Without dose correction, the area under the plasma concentration-time curve (AUC) for the quinidine gluconate form was 85 per cent that of the solution: an amount equivalent to the relative actual amount of quinidine base in the quinidine gluconate dosage form. The maximum plasma concentration (Cmax), Cmin, peak-to-trough differences, and AUC from the quinidine sulfate extended-release form given 300 mg q12h were similar to the solution given 150 mg q6h. With dose correction, the quinidine gluconate controlled-release form given q12h had equivalent AUC but larger peak-to-trough differences than either the quinidine sulfate extended-release product given q12h or quinidine sulfate in solution given q6h.

Adult↗

PubMed1990

Low dose quinidine-mexiletine combination therapy versus quinidine monotherapy for treatment of ventricular arrhythmias.

Low dose quinidine-mexiletine combination therapy was compared with quinidine monotherapy in 15 patients with frequent ventricular premature complexes and nonsustained ventricular tachycardia in a dose escalation cross-over study. Oral combination therapy was initiated with quinidine gluconate (165 mg) plus mexiletine (150 mg) every 8 h. If ventricular premature complexes were not suppressed greater than or equal to 80% and nonsustained ventricular tachycardia greater than or equal to 90%, the dose was increased to a maximum of 330 mg of quinidine plus 200 mg of mexiletine. Quinidine monotherapy was initiated with 330 mg and escalated to a maximum of 660 mg every 8 h if criteria for effectiveness were not met. Combination quinidine-mexiletine therapy suppressed 80% of ventricular premature complexes in 13 of 14 patients and suppressed 100% of episodes of ventricular tachycardia in 6 of 8 patients (mean quinidine dose 200 +/- 70 mg; mean mexiletine dose 146 +/- 24 mg every 8 h). The mean effective trough quinidine and mexiletine concentration was 1.0 +/- 0.7 and 0.9 +/- 0.4 microgram/ml, respectively. Monotherapy was less effective; that is, greater than or equal to 80% suppression of ventricular premature complexes was observed in 5 of 15 patients and 100% suppression of ventricular tachycardia in 2 of 9 patients. The mean quinidine monotherapy dose was 462 +/- 155 mg every 8 h; the mean quinidine concentration was 1.8 +/- 0.8 microgram/ml. Adverse systemic effects occurred in 3 patients on quinidine-mexiletine therapy and in 11 on quinidine monotherapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗

PubMed1990

Role of quinidine in the mexiletine-quinidine interaction: electrophysiologic correlates of enhanced antiarrhythmic efficacy.

Quinidine has multiple electrophysiologic effects, including prolongation of ventricular conduction time, repolarization, and refractoriness. The purpose of this study was to address the relative contributions of these electrophysiologic effects to the enhanced anti-arrhythmic activity observed when quinidine is combined with mexiletine. We compared antiarrhythmic and electrophysiologic effects observed when quinidine or its stereoisomer quinine were combined with mexiletine. Quinine and quinidine both prolong conduction time; however, these agents have divergent effects on ventricular repolarization time and refractoriness. The modest prolongation of conduction time observed with quinine and mexiletine-quinine in the absence of change of ventricular refractoriness was not associated with antiarrhythmic efficacy. The antiarrhythmic efficacy of mexiletine-quinidine exceeds that of mexiletine-quinine, suggesting that the ability of quinidine to prolong refractoriness and repolarization contributes to the antiarrhythmic efficacy of mexiletine-quinidine. Although, both the mexiletine-quinidine combination and quinidine monotherapy prolonged refractoriness to a similar extent, the mexiletine-quinidine combination produced greater antiarrhythmic efficacy and prolonged interventricular conduction within the periinfarct zone to an extent greater than did quinidine alone. We concluded that the role of quinidine in producing enhanced antiarrhythmic activity when combined with mexiletine includes both prolongation of refractoriness and conduction time in the periinfarct zone.

Action Potentials↗

PubMed1994

Usefulness of oral quinidine-mexiletine combination therapy for sustained ventricular tachyarrhythmias as assessed by programmed electrical stimulation when quinidine monotherapy has failed.

In patients presenting with sustained ventricular tachyarrhythmias, when oral quinidine monotherapy fails as determined by programmed electrical stimulation, the degree of benefit observed with combination therapy with mexiletine is debated. We prospectively studied 20 consecutive patients (16 men and 4 women) aged 33 to 77 years (mean age, 62 +/- 11 years) who were treated with maximally tolerated quinidine and mexiletine combination therapy and who had ventricular tachyarrhythmias induced at baseline and during oral quinidine monotherapy. Coronary artery disease was present in 19 patients (95%). Programmed electrical stimulation was performed at 2 drive train cycle lengths with up to 3 extrastimuli at two ventricular sites. During follow-up study with combination quinidine-mexiletine therapy ventricular tachyarrhythmias were rendered noninducible in four patients (20%). The remaining 16 patients showed a significant slowing of their tachycardia cycle length (267 +/- 56 msec baseline vs 320 +/- 75 msec with quinidine vs 345 +/- 53 msec with combination therapy, p < 0.05). There was also an increase in the mean QTc interval (452 +/- 50 msec baseline vs 477 +/- 79 msec after quinidine vs 486 +/- 65 msec with combination quinidine-mexiletine therapy, p = not significant) and in the mean ventricular effective refractory period (246 +/- 25 msec baseline vs 281 +/- 37 msec after quinidine vs 290 +/- 25 msec with combination quinidine-mexiletine therapy, p < 0.05). We conclude that sustained ventricular tachyarrhythmias induced during quinidine monotherapy were rendered noninducible by oral combination therapy with quinidine-mexiletine in 20% of cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

Electrophysiological interactions between quinidine-lidocaine and quinidine-phenytoin in guinea-pig papillary muscle.

The interactions between quinidine and lidocaine or phenytoin at the sodium channel level have been studied in the present work. The maximum upstroke velocity (Vmax) of the guinea-pig papillary muscle action potential has been used as a measure of the sodium current. Lidocaine interfered with the use-dependent blocking effects on Vmax of quinidine, by decreasing the fraction of sodium channels blocked by quinidine during the conditioning action potential, in an apparently competitive way. These results strongly suggest that quinidine and lidocaine bind to a common receptor site. Alternatively, it has been suggested that lidocaine and quinidine bind to different but related receptor sites, since lidocaine may induce allosteric changes in quinidine's receptor. Phenytoin increased the use-dependent blocking effects on Vmax of quinidine by slowing the time course of the slow component of reactivation of Vmax induced by quinidine. Phenytoin did not change the fraction of sodium channels blocked by quinidine during the conditioning action potential. These results suggest that phenytoin binds to a different receptor site than quinidine.

Action Potentials↗

PubMedDate not supplied

Pharmacokinetics and pharmacodynamics of quinidine and its metabolite, quinidine-N-oxide, in beagle dogs.

Quinidine and one of its major metabolites, quinidine-N-oxide, were given by separate i.v. infusions to each of three beagle dogs. Plasma and urine samples were analysed for pharmacokinetic comparison of the drug and its metabolite. Quinidine apparently distributed into two major compartments, while the N-oxide distributed into three compartments. The compartment-independent pharmacokinetic parameters (mean +/- SD) were for quinidine Vdss 4.78 +/- 1.11 l/kg, clearance 0.074 +/- 0.047 l/min, terminal half-life 720 +/- 343 min and for quinidine-N-oxide Vdss 1.03 +/- 0.21 l/kg, clearance 0.065 +/- 0.012 l/min, terminal half-life 316 +/- 69 min. Only 29% of quinidine was recovered in the urine as unchanged drug while 77% of the N-oxide was excreted unchanged via the kidney. Non-linear renal elimination of the N-oxide was observed in two out of three dogs with a Michaelis-Menten constant, KM of about 7 micrograms/ml (21 microM). Prolongation of the QT-interval in the ECG response was used for comparing pharmacodynamic effects. Quinidine was about three to four fold more active than the N-oxide at similar plasma concentrations. Quinidine-N-oxide concentrations in plasma after quinidine administration were very low and would not contribute significantly to the quinidine effect.

Animals↗

PubMed1981

[Relationship between quinidine plasma level and clinical effect for a new quinidine retard-formulation (author's transl)].

To convert atrial fibrillation 19 patients (8 male and 11 female) were administered (5-vinyl-2-quinuclidinyl)-(6-methoxy-4-quinolyl)-methanol, a new slow-release quinidine formulation (Chinidinorm), containing 250 mg quinidine bisulphate x 4 H2O per tablet, corresponding to 200 mg quinidine sulphate or 164 mg quinidine base respectively. After careful titration of the effective dosage sinus rhythm could be obtained in 17 patients and auriculo-ventricular rhythm in one patient. The drug failed only in one female patient for the occurrence of diarrhoea. Minimum as well as maximum quinidine levels measured in plasma correlated significantly to the quinidine dosages/kg b.w. administered. Part of the quinidine concentrations measured in plasma was at or under the minimum effective levels, respectively, in literature. According to our results it should therefore be discussed to slightly reduce the lower limit of efficacy for plasma quinidine levels. The new quinidine formulation proved to be effective and poor of side-effects with little variations in effective plasma level. Therefore it is to be considered equivalent to all quinidine retard-formulations on the market at present.

Adult↗

PubMed1983

Electrophysiological effects of quinidine alone and of the combination quinidine-verapamil on AV conduction in humans.

The influence of 320 mg quinidine administered intravenously (i.v.), as well as subsequent administration of 5 mg verapamil i.v. on atrioventricular conduction was studied in 8 patients during sinus rhythm and atrial stimulation with the aid of His bundle electrography. Among the electrophysiologic parameters of the atrium the sinus rate increased significantly after quinidine and again increased slightly after subsequent administration of verapamil. During sinus rhythm the PA interval was not influenced by either substance. Conversely, during atrial stimulation the STA interval increased significantly under the effect of quinidine, while verapamil had no further influence. As an indicator of conduction time in the AV node, the AH interval was decreased significantly by quinidine during sinus rhythm and atrial stimulation. This effect was significantly counteracted by the additional administration of verapamil. The HV interval as a measure of the His-Purkinje conduction was not significantly affected. The QRS duration was increased significantly by quinidine and was not further influenced by verapamil. The QTc and QT intervals increased significantly after administration of quinidine and were again slightly, but significantly shortened by verapamil. Our investigations show that the combination of quinidine and verapamil, which has clinically been found to have a higher conversion rate than quinidine alone, is well justified from an electrophysiologic point of view and that undesirable quinidine-related effects, such as rapid AV conduction in cases of atrial fibrillation and flutter, can be avoided by the subsequent administration of verapamil.

Adult↗

PubMed1995

Comparison of sotalol with digoxin-quinidine for conversion of acute atrial fibrillation to sinus rhythm (the Sotalol-Digoxin-Quinidine Trial).

We randomized 61 patients with paroxysmal atrial fibrillation (AF) ( < 48 hours from onset) to either sotalol or quinidine treatment. Conversion of rhythm was recorded by Holter monitoring. The starting 80 mg dose of sotalol was repeated at 2, 6, and 10 hours if AF persisted (heart rate > 80 beats/min), and if systolic blood was > or = 120 mm Hg. In the quinidine group, if heart rate > 100 beats/min, it was decreased with intravenous digoxin, whereafter 200 mg of oral quinidine sulfate was given maximally 3 times, each dose 2 hours apart. Conversion of AF to sinus rhythm occurred in 17 or 33 patients (52%) taking sotalol, and in 24 of 28 patients (86%) taking quinidine (p < 0.0001). Electric cardioversion was necessary in 39% of the former and in 14% of the latter group. The mean delay from first trial drug to sinus rhythm with the trial medication was 10.2 +/- 7.6 hours in the sotalol group and 4.0 +/- 2.9 hours in the quinidine group (p < 0.01). Treatment was discontinued in 16 patients taking sotalol (48%) because of asymptomatic bradycardia or hypotension, and in 20 taking quinidine (71%) because of rhythm conversion. Asymptomatic wide complex tachycardia (QRS > 0.12 second) was found in 13% and 27% of patients taking sotalol and quinidine, respectively. The longest RR intervals were 6.4 and 3.8 seconds in the sotalol and quinidine groups, respectively. Oral sotalol did not appear as effective as quinidine sulfate treatment in conversion of paroxysmal AF.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMed1997

Cardiac effects of quinidine on guinea-pig isolated perfused hearts after in vivo quinidine pretreatment.

1 Experimental and clinical studies suggest that class I and class III antiarrhythmic drugs may be subject to pharmacological tolerance during long term treatment, leading to loss of therapeutic effectiveness. 2 The aim of this study was to ascertain whether prolonged in vivo treatment with the Class Ia agent quinidine can modify cardiac (electrical and mechanical) responses to the drug. 3 A group of guinea-pigs (n = 7) was treated intraperitoneally (q.d.) for 6 days with 75 mg kg-1 quinidine sulphate. Preliminary pharmacokinetic experiments indicated that this dose could attain Plasma concentrations similar to those that are therapeutic in man (2-5 mg l-1). A control group (n = 7) received a saline solution for the same period. 4 Twenty-four hours after the last administration hearts were removed and retrogradely perfused at constant flow (stimulation frequency: 2.5 Hz). The following parameters were measured: maximal derivative of intraventricular pressure (dP/dtmax); coronary perfusion pressure (Cp); PR, QRS and JT intervals, on surface ECG. The effects of quinidine on these parameters were measured at different concentrations (2, 4, 8, 12, 16, 20 microns) and compared in the two experimental groups. 5 In the group quinidine decreased in a dose-dependent manner dP/dt and increased PR and QRS intervals. JT interval was increased at the lowest concentrations and decreased at the highest (biphasic effect). Cp did not change significantly. 6 In the pretreated group quinidine qualitatively produced the same effects on dP/dt and ECG intervals as in control group. Also the magnitude of these effects was not significantly different between the two groups. In contrast with findings in control experiments. Cp was significantly decreased by increasing quinidine concentration. Mean baseline Cp was higher in pretreated than in the control group (though not significantly, P = 0.072) and quinidine addition abolished this difference. Thus, it is suggested that quinidine withdrawal induced a rebound increase in coronary tone, due to the unmasking of vasoconstrictor homeostatic mechanisms elicited by the in vivo vasodilating effect of the drug. 7 In conclusion, our data do not support the possibility that tolerance ensues during long term quinidine treatment, at least as far as electrophysiological and contractility effects are concerned. Further experimental work is needed to explain the appearance of a coronary vasodilating effect in pretreated hearts.

Animals↗

PubMed1997

Effectiveness of verapamil-quinidine versus digoxin-quinidine in the emergency department treatment of paroxysmal atrial fibrillation.

STUDY OBJECTIVE: To determine the relative effectiveness of a verapamil-quinidine sequential combination versus digoxin-quinidine in the emergency department treatment of paroxysmal atrial fibrillation (PAF). METHOD: This prospective, double-blind, randomized, controlled trial involved patients, aged 18 to 75 years, with new-onset (< 48 hours) atrial fibrillation who presented to a community-based urban hospital with an annual ED census of 65,000. Exclusion criteria included ventricular response rate lower than 100 or higher than 200 beats/minute, allergy to study drugs, hypotension with evidence of end-organ hypoperfusion, and conduction abnormalities. Consenting patients were randomly assigned to receive rapid digitalization (1.0 mg over 2 hours) or i.v. verapamil (sequential 5-mg boluses up to 20 mg). After ventricular rate was controlled (< 100 beats/minute), oral quinidine (200 mg) was initiated and repeated every 2 hours until conversion to normal sinus rhythm (NSR) occurred, until 1 g of quinidine was administered, or until adverse effects supervened. Heart rate, blood pressure, cardiac rhythm, time to conversion, and adverse effects were documented. RESULTS: Forty-four patients received the study drugs. Three were withdrawn, leaving 19 in the verapamil-quinidine (VER-Q) group and 22 in the digoxin-quinidine (DIG-Q) group. Sixteen patients (84%) in the VER-Q group and 10 (45%) in the DIG-Q group converted to NSR within 6 hours (P < .02). Mean time to conversion (+/-SD) was 185 +/- 146 minutes for VER-Q and 368 +/- 386 minutes for DIG-Q patients (P = NS). Twelve VER-Q patients (63%) and 6 DIG-Q patients (27%) were discharged from the ED (P < .05). Minor adverse effects were more common in the VER-Q group. No mortality or significant morbidity occurred. CONCLUSION: The sequential combination of verapamil and quinidine, in the doses studied, is an effective treatment for PAF and is superior to digoxin-quinidine. Digoxin should no longer be considered the treatment of choice for uncomplicated PAF.

Adult↗

PubMedDate not supplied

Relative bioavailability of quinidine gluconate and quinidine sulfate in healthy volunteers.

A comparison of the bioavailability of quinidine sulfate to quinidine gluconate tablets in a single-dose randomized cross-over design with 20 healthy volunteers shows that the sulfate salt is more rapidly absorbed and provides significantly greater peak concentrations 1 hour after administration as compared to the peak levels achieved with the gluconate salt at approximately 5 hours after administration. When adjusted for the actual amount of quinidine contained in each tablet, there was no significant difference in the amount of quinidine bioavailable. Since quinidine gluconate absorption is significantly slower than quinidine sulfate, a combination of the two dosage forms may be utilized in providing the loading dose. Based on the computer modeling and the clinical data accumulated by this laboratory (unpublished) over the past four years, quinidine gluconate, in the dosage form utilized in this study, provides more constant blood levels with smaller differences between the Cpmax and Cpmin than the sulfate when administered every 6 or 8 hours. Further controlled clinical studies are needed to confirm these observations in patients.

Adult↗

PubMedDate not supplied

Bioavailability of a commercial sustained-release quinidine tablet compared to oral quinidine solution.

The bioavailability of quinidine sulfate after oral administration of a commercial sustained-release quinidine tablet was compared with that of oral quinidine sulfate solution in 18 normal subjects. Three hundred milligrams of each product was administered to each subject in standard cross-over fashion on separate occasions, with plasma quinidine levels measured for 46 h after each dose. Although peak plasma quinidine levels were lower, and occurred later, after tablet administration than after solution, analysis of the area under the plasma quinidine level-time curve (AUC) values for each product indicated that the products were equivalent, in terms of the extent of absorption, with the mean AUC (0-46 h) value for the tablet, 8744 . 4 ng x h ml-1, comparable to that of the solution, 9145 . 9 ng x h ml-1.

Administration, Oral↗

PubMed2000

Stereospecificity of antibody: quinine, the optical isomer of quinidine and anti-malarial drug chloroquine do not cross-react with quinidine immunoassays.

Quinine is an optical isomer of quinidine. Both quinine and chloroquine (an aminoquinoline derivative) are used in treating malaria. The authors studied cross-reactivity of quinine and chloroquine with the quinidine immunoassays using the TDx and AxSYM analyzers (Abbott Laboratories, Abbott Park, IL). The authors observed no cross-reactivity of chloroquine with quinidine immunoassays (TDx and AXSYM) even when drug-free serum was supplemented with 1000 microg/mL chloriquine. The authors observed no cross-reactivity of quinine up to a concentration of 250 microg/mL. At higher concentrations, the authors observed a small cross-reactivity. The cross-reactivity of a substance should be studied in the presence of the primary analyte. When serum pools prepared from patients receiving quinidine were supplemented with various concentrations of quinine or chloroquine, the authors observed statistically significant declines in quinidine concentrations with higher concentrations of both quinine and chloroquine. The authors observed significant cross-reactivity of L-amphetamine with the amphetamine immunoassay also marketed by Abbott Laboratories and run on the AxSYM analyzer. The authors conclude that although the antibody used in the quinidine assay is stereospecific, the antibody used in the amphetamine assay by the same manufacturer is not stereospecific.

Antibodies↗