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PubMed2005

Transport of the dopamine D2 agonist pramipexole by rat organic cation transporters OCT1 and OCT2 in kidney.

We investigated the mechanism of renal tubular secretion of the dopamine D2 receptor agonist pramipexole in rats, focusing on organic cation transporters 1 and 2. The uptake of [14C]pramipexole by Xenopus oocytes injected with complementary RNA of either rat organic cation transporter (rOCT) 1 or rOCT2 was significantly higher than that by water-injected oocytes: the kinetic parameters, K(m) and V(max), of pramipexole uptake were 49.5 muM and 234 pmol/60 min/oocyte for rOCT1, and 16.9 microM and 12.8 pmol/60 min/oocyte for rOCT2. Pramipexole was taken up into kidney slices in a time- and concentration-dependent manner, and Eadie-Hofstee plots revealed the involvement of two saturable components. The kinetic parameters, K(m1) and V(max1), of the high-affinity component were 12.9 microM and 10.7 nmol/15 min/g kidney, respectively. The uptake of [14C]pramipexole by rOCT1, rOCT2, and kidney slices was inhibited by procainamide and corticosterone, which are selective inhibitors of rOCT1 and rOCT2, respectively. The IC50 values of procainamide and corticosterone for the uptake of [14C]pramipexole by rOCT1, rOCT2, and kidney slices were 7.7, 167.0, and 47.0 microM and 163.7, 10.7, and 47.7 microM, respectively. These results demonstrate that both rOCT1 and rOCT2 are involved in the renal uptake of pramipexole across the basolateral membrane of the proximal tubular epithelial cells.

Amantadine↗
PubMed1992

Neurogenic vasodilator control of rabbit ear blood flow.

Ear blood flow subserves thermoregulation in the rabbit. The purpose of this study was to determine if the increase in rabbit ear blood flow, in response to increases in internal temperature (Ti) of approximately 2 degrees C (38.0-40.0 degrees C), is due to an active vasodilation or a withdrawal of adrenergic vasoconstrictor activity. New Zealand White rabbits were chronically instrumented with a pulse Doppler flow probe on the central ear artery of the left and right ear for the measurement of ear blood flow velocity (EBF, kHz). Catheters were also positioned in one occipital artery for selective administration of an alpha 1-adrenergic antagonist to one ear, while the contralateral ear served as a control. During hyperthermia (H) (increase in rectal temperature) alpha 1-adrenergic blockade had no effect on the maximum EBF (5.95 +/- 0.87 before vs. 6.11 +/- 1.04 kHz after). However, alpha 1-adrenergic blockade increased resting EBF during normothermia from 0.18 +/- 0.04 to 1.23 +/- 0.27 kHz (P less than 0.05), suggesting that a decrease in alpha 1-adrenergic tone may account for approximately 20% of the increase in EBF during heating. The second protocol was designed to determine if blockade of the auricular nerve would alter EBF response to H. During maximum EBF during H, saline or procainamide was injected in the tissue surrounding the auricular nerve. Injection of procainamide decreased EBF from 5.99 +/- 0.87 to 0.48 +/- 0.19 kHz, while injection of saline had no effect on EBF of the contralateral ear (4.33 +/- 1.16 before vs. 3.97 +/- 1.04 kHz after).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1984

Verapamil in ventricular tachycardia.

We compared the effects of verapamil to high dose procainamide on the rate of inducible and spontaneously occurring ventricular tachycardia (VT) in 10 patients. Verapamil induced a significant increase in the rate of tachycardia (R-R interval decreased from 278 +/- 54 to 233 +/- 32 ms, mean +/- SD; p less than 0.025 by paired t test) while procainamide slowed the tachycardia (mean R-R interval was 328 +/- 72 ms, p less than 0.02). Verapamil prevented the induction of sustained VT and was effective as chronic oral antiarrhythmic therapy in 2 patients. The accelerated VT culminated in ventricular fibrillation in 1 patient. It is assumed that verapamil may have either increased conduction velocity or shortened the reentrant cycle. This may be related either to a primary effect of the drug or secondary to increased catecholamine stimulation due to a vasodilatory effect.

Adolescent↗
PubMedDate not supplied

Hemodynamic changes during cardioversion in utero: a case report of supraventricular tachycardia and atrial flutter.

Two cases of fetal tachyarrhythmias were treated in utero. One case showed supraventricular tachycardia which was successfully treated with procainamide. The other case was an atrial flutter with 2:1 atrioventricular conduction (AVC) which was treated with digoxin and verapamil. In both cases, the blood flow in the descending aorta was observed using pulsed Doppler ultrasound during therapy. In the first case, the interval of blood flow peaks was suddenly prolonged to normal heart rate, and in the second case, the blood flow peaks appeared irregularly which indicated that (AVC) was intermittently blocked. The blood flow pattern represented the mode of cardioversion. The blood flow velocity was also measured in both cases; it decreased transiently during therapy representing a depression in cardiac function. The cause of this was thought to be the negative inotropic effects of procainamide and verapamil. In spite of these negative inotropic effects, a greater R-R interval means a greater stroke volume. This relationship has a favorable effect on the fetal circulation as a result of therapy for fetal tachyarrhythmias.

Adult↗
PubMed1976

Electrophysiologic properties and response to pharmacologic agents of fibers from diseased human atria.

We used standard microelectrode techniques to record action potentials of human right atrial fibers obtained during cardiac surgery, and correlated these potentials with clinical and preoperative ECG data. Human atrial fibers were classified as follows: Group A (ten patients) had a maximum diastolic potential (MDP) of -71.4 +/- 5.1mV (mean +/- SD), and action potentials that were primarily fast responses. These atria were normal or slightly dilated. In group B (12 patients) MDP was 50.3 +/- 5.7 mV; action potentials were slow responses and the atria were moderately to markedly dilated. Atrial arrhythmias occurred in four group B and no group A patients. The ECG revealed a signficant difference (P less than 0.005) in P wave duration: group A, 89 +/- 3.0 msec; group B, 111 +/- 6.0 msec. Verapamil, 0.1 mg/L, markedly depressed only the action potential plateau of group A. Procainamide 1-100 mg/L had equivalent effects on fibers of both groups A and B, effects which were small at dosages of less than 40 mg/L. Procainamide did not depress slow response automaticity, but verapamil (0.1-1 mg/L) did.

Action Potentials↗
PubMed1981

Torsades de pointes: electrophysiologic studies in patients without transient pharmacologic or metabolic abnormalities.

Electrophysiologic studies were performed in 21 patients who had torsades de pointes. This ventricular tachyarrhythmia, characterized by rapid (200-250 beats/min) and irregular paroxysms and progressively varying QRS amplitude and polarity, occurred in the absence of electrolyte disturbance, antiarrhythmic drug therapy or acute ischemia. The QTc interval was prolonged in seven of 21 patients. Electrophysiologic study included ventricular pacing with the introduction of one to three extrastimuli and rapid ventricular pacing. The effect of i.v. procainamide or quinidine in these patients was also studied. Torsades de pointes was inducible n 19 of 21 patients. Induced episodes closely resembled spontaneous episodes. Torsades de pointes spontaneously progressed to ventricular tachycardia with a uniform morphology in three patients and to ventricular fibrillation in four. In eight patients, procainamide or quinidine converted torsades de pointes into typical reentrant ventricular tachycardia. Our data suggest that torsades de pointes in this setting may be a rapid reentrant ventricular tachycardia closely related to recurrent sustained ventricular tachycardia and a precursor to ventricular fibrillation and sudden death.

Adult↗
PubMed1984

Dynamic variability of binding of antiarrhythmic drugs during the evolution of acute myocardial infarction.

We tested the hypothesis that the changes in free fatty acid and alpha 1-glycoprotein concentrations, which occur during acute myocardial infarction, exert asynchronous and opposing influences on the serum protein binding of selected drugs. Free drug fractions of two antiarrhythmic agents with contrasting binding characteristics, quinidine and procainamide, were related to free fatty acid and alpha 1-glycoprotein concentrations on days 1 through 5 and 10 in 20 patients with acute myocardial infarction. The mean free quinidine fraction was elevated on day 1 (9.0 +/- 4.4% vs 6.7 +/- 2.7% in patients with stable heart disease; p less than .05) and fell progressively to day 10 (4.0 +/- 2.8%; p less than .0002) as free fatty acid concentration decreased (day 1 = 464 +/- 272 meq/liter; day 10 = 264 +/- 155 meq/liter; p less than .01) and alpha 1-glycoprotein concentration increased (day 1 = 98 +/- 31 mg/dl; day 10 = 141 +/- 47 mg/dl; p less than .02). Multiple stepwise regression showed a major influence of changing alpha 1-glycoprotein concentration on the observed sequential changes in the free quinidine fraction (p less than .005). In contrast, no serial changes in procainamide binding were noted. In conclusion, metabolic changes during the course of acute myocardial infarction sequentially alter free quinidine fraction and, consequently, may influence pharmacodynamics.

Aged↗
PubMed2002

Clinical and molecular heterogeneity in the Brugada syndrome: a novel gene locus on chromosome 3.

BACKGROUND: Brugada syndrome is a form of idiopathic ventricular fibrillation characterized by a right bundle-branch block pattern and ST elevation (STE) in the right precordial leads of the ECG. Sodium channel blockers increase STE. Mutations of the cardiac sodium channel SCN5A cause the disorder, and an implantable cardioverter-defibrillator is often recommended for affected individuals. Mutations in other genes have not been identified, and it is not known if the efficacy of drug testing or the malignancy of arrhythmias correlates to the gene defect. METHODS AND RESULTS: We performed histories, physical examinations, ECGs, and drug testing on a large multigenerational family with Brugada syndrome. DNA isolated from blood samples, polymorphic genomic markers, and polymorphisms within candidate sodium channels were used for a genome-wide screen, fine mapping, and linkage analysis. We identified 12 affected individuals (right bundle-branch block, > or =1-mm STE) with an autosomal dominant inheritance pattern characterized by incomplete penetrance that appeared to be dependent on age and sex. Four affected individuals had syncope and 2 had documented ventricular arrhythmias, but there was minimal family history of sudden death. Procainamide infusions did not identify additional affected individuals. Linkage was present to an approximately equal 15-cM region on chromosome 3p22-25 (maximum LOD score=4.00). The sodium channel genes SCN5A, SCN10A, and SCN12A on chromosome 3 were excluded as candidates (LOD scores < or =-2). CONCLUSIONS: A Brugada syndrome locus distinct from SCN5A is associated with progressive conduction disease, a low sensitivity to procainamide testing, and a relatively good prognosis in a single large pedigree.

Adult↗
PubMed1991

Drug-induced anti-histone autoantibodies display two patterns of reactivity with substructures of chromatin.

Increasing evidence suggests that autoantibodies in the rheumatic diseases are a consequence of immune selection by self-material, but the nature of the in vivo immunogen is unknown. Insight into this problem may be obtained by measuring autoantibody binding to various forms of a target antigen. Antihistone antibodies arising as a side effect of therapy with various drugs offer an opportunity to explore this premise because many forms of histone have been characterized and adapted to ELISA formats. Two patterns of antibody reactivity were observed. All 21 patients with symptomatic procainamide-induced lupus and 7 of 12 patients with quinidine-induced lupus had IgG antibodies reacting predominantly with the (H2A-H2B)-DNA complex and with chromatin. In contrast, antibodies in 19 of 24 patients taking procainamide without accompanying lupus-like symptoms did not show any pattern. The second pattern was observed in 18/19 chlorpromazine-treated patients and 14/17 patients with hydralazine-induced lupus in which IgM antibodies displayed more reactivity with DNA-free histones than with the corresponding histone-DNA complexes and almost no binding to H1-stripped chromatin. Absorption studies were entirely consistent with these results. Thus, the two patterns of reactivity with nucleosomal components reflect the molecular substructure of chromatin, suggesting that two processes underlie antihistone antibody induction by drugs. In one, IgG autoantibodies appear to be elicited by chromatin, whereas in the other, autoimmune tolerance to native chromatin appears largely intact, and IgM antibodies may be driven by DNA-free histone.

Autoantibodies↗
PubMed2004

Drug-drug interactions between antiarrhythmic drugs in chick embryos.

The drug-drug interactions between antiarrhythmic drugs were studied in chick embryos. Fertilized eggs of White Leghorns were incubated and investigated. Procainamide or flecainide with and without propranolol was injected into the air sac of a fertilized egg. Electrocardiograms (ECGs) were recorded 0 to 60 min after the injection. After each drug injection alone, the heart rate was not different compared with the control. However, the heart rate was significantly decreased by combinations of procainamide and propranolol or flecainide and propranolol. In addition, arrhythmia was produced in combination with propranolol. These findings indicate that the drug-drug interactions between antiarrhythmic drugs have a marked influence on the heart rate in chick embryos.

Animals↗
PubMed1994

Amelioration of postischemic reperfusion injury by antiarrhythmic drugs in isolated perfused rat lung.

Antiarrhythmic drugs, such as lidocaine, quinidine, and procainamide, have been shown to be effective against postischemic reperfusion injury in isolated rat lungs. Rat lungs were perfused at a constant flow with Krebs-Henseilet buffer supplemented with 4% bovine serum albumin and ventilated with air containing 5% CO2. The lungs were subjected to ischemia by stopping perfusion and ventilation for 60 min followed by 30 min of reperfusion. Lung injury was determined by measuring the increase in wet-to-dry lung weight ratio, while pulmonary arterial pressure and peak airway pressure were calculated from the pre- and postischemic differences. Lidocaine, quinidine, and procainamide at doses of 5, 10, and 20 mg/kg body weight, respectively, were found to attenuate the postischemic lung injury significantly (p < 0.0001). The formation of cyclooxygenase products, which were elevated during reperfusion, was also significantly (p < 0.0001) inhibited by these drugs. Since these antiarrhythmic agents are found to be powerful scavengers of hydroxyl radicals and can prevent membrane lipid peroxidation, these findings suggest that the antioxidant properties of these drugs may, in part, be responsible for protecting the lungs against reperfusion injury.

Animals↗
PubMed1992

Drug-induced lupus pleuritis mimicking pleural space infection.

A 78-year-old man presented with acute lupus pleuritis due to procainamide. The pleural fluid was a turbid, yellow exudate with a WBC count of 53,200/cu mm (70 percent polymorphonuclear leucocytes), LDH of 4,296 IU/L, and pH of 7.195. Although these fluid characteristics suggested pleural space infection, they were due to pleural inflammation from drug-induced lupus. LE cells were present in the fluid and results of microbiologic studies were negative. Clinical and roentgenographic improvement followed discontinuation of procainamide.

Acute Disease↗
PubMed1993

Ischemically mediated sustained monomorphic ventricular tachycardia. Resolution with anti-ischemic therapy.

We describe a patient with ischemically mediated sustained monomorphic ventricular tachycardia occurring at rest and resistant to treatment with intravenously administered procainamide. Percutaneous transluminal coronary angioplasty was initially successful, but rest angina and ventricular tachycardia, resistant to procainamide therapy, recurred 2 weeks later and responded to aggressive anti-ischemic medical therapy. We suggest that anti-ischemic medication may be of benefit in patients with malignant ventricular arrhythmias precipitated by spontaneous myocardial ischemia.

Coronary Angiography↗
PubMed1976

Absence of blocking effect of quinidine on responses to norepinephrine in the isolated dog atrium.

The isolated right dog atrium was perfused through the sinus node artery with blood led from a heparinized support dog under constant perfusion pressure of 100 mmHg. The positive chronotropic and inotropic responses to norepinephrine were not significantly suppressed by treatment with large amounts of quinidine or procainamide, but completely blocked by propranolol. From these results, it was demonstrated that quinidine and procainamide have no adrenergic beta-blocking activity on chronotropism and on inotropism in the heart.

Adrenergic beta-Antagonists↗
PubMed1983

Intropic effects of several antiarrhythmic drugs.

The effects of intravenous administration of several quinidine-like antiarrhythmic drugs (bunaftine, monochloroacetyl ajmaline, lidocaine, mexiletine, disopyramide, aprindine, diphenylhydantoin, procainamide) on left ventricular performance, evaluated by systolic time intervals (STI), were studied in 100 patients with atherosclerotic heart disease. The STI were measured: the pre-ejection period (PEP), the isometric contraction time (ICT), the left ventricular ejection time (LVET), corrected LVET (LVETc), and the PEP/LVET ratio. The degree of impairment of left ventricular performance was maximal after aprindine and disopyramide administration. This was demonstrated by significant increases in the PEP, ICT, and PEP/LVET and by significant decreases in LVET and LVETc, in patients in both III-IV and I-II NYHA classes. Bunaftine, monochloroacetyl ajmaline, and lidocaine induced a less marked impairment of myocardial performance, since the PEP, ICT, and PEP/LVET increases were not significant compared to controls in patients in NYHA class I-II, and since no variation of LVET and LVETc were observed. Mexiletine effects on myocardial performance appear to be intermediate between these groups of drugs. Diphenylhydantoin and procainamide, considered separately because of their effects on heart rate and blood pressure which are not possessed by the other drugs, induced significant increases of PEP in NYHA class III-IV patients. However, the effects of these 2 drugs on myocardial performance may have been underestimated, due to the concomitant hemodynamic effect of these drugs.

Ajmaline↗
PubMed1989

Treatment of atrial flutter and rapid atrial tachycardia with transesophageal atrial pacing.

Eight patients with atrial flutter (AF) and rapid atrial tachycardia (AT) (5 common AF, 1 uncommon AF and 2 AT) were treated with transesophageal atrial pacing (TEAP). In 5 patients no antiarrhythmic agent was used during this study, and in 3 patients procainamide was administrated intravenously. Conversion to sinus rhythm was successfully achieved in 7 patients (5 common AF and 2 AT). Two patients were converted to sinus rhythm immediately after pacing, and transient atrial fibrillation was induced before conversion to sinus rhythm in 5 patients. TEAP failed to terminate the arrhythmia in 1 patient with uncommon AF. Administration of procainamide reduced the atrial rate in 2 common AF and 1 AT, which were successfully converted to sinus rhythm by TEAP, but induced a rapid ventricular response in 2 patients, one of whom also developed hypotension before conversion. No significant complication due to TEAP was observed in this study. In conclusion, TEAP is a noninvasive method with fewer complications and has nearly the same high efficacy for converting AF and rapid AT to sinus rhythm as DC cardioversion or transvenous atrial pacing.

Aged↗
PubMed1985

Cardiovascular and respiratory effects of antiarrhythmic drugs on conscious beagles.

Cardiovascular effects of antiarrhythmic drugs and their effects on the respiratory rate were examined in conscious beagles. Disopyramide, 1.5 mg/kg i.v., increased the blood pressure and decreased the heart rate, but higher dose of 5 mg/kg i.v. increased both. Disopyramide showed no central nervous side effects. Procainamide, 20 and 60 mg/kg i.v., increased the blood pressure and heart rate without changing the respiratory rate. A higher dose (60 mg/kg i.v.) of procainamide induced vomiting. Lidocaine, 2 and 6 mg/kg i.v., and phenytoin, 3 and 10 mg/kg i.v., simultaneously increased the blood pressure, heart rate and respiratory rate accompanied by excitement, and with a higher dose (6 mg/kg i.v.) of lidocaine, by convulsions. Verapamil, 0.1 and 0.3 mg/kg i.v., induced tachycardia without serious neurological effects. In conscious healthy dogs cardiovascular depressant actions of antiarrhythmic drugs could only rarely be observed.

Animals↗
PubMed1990

Acecainide (N-acetylprocainamide). A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in cardiac arrhythmias.

Acecainide (N-acetylprocainamide), the N-acetylated metabolite of procainamide, is a Class III antiarrhythmic agent. It can be given either intravenously or orally, and is eliminated primarily by renal excretion. In a small number of noncomparative and placebo-controlled short term therapeutic trials acecainide markedly reduced premature ventricular beats and prevented induction of ventricular tachycardia in more than 70% of patients following intravenous administration and in about 50% after oral administration. Acecainide was effective in about one-quarter of patients refractory to other antiarrhythmic drugs. Interpretation of its effectiveness following long term oral therapy is complicated by the limited number of patients, and patients discontinuing due to adverse effects or lack of efficacy. However, about 40% of the small number treated for extended periods were controlled for periods of 6 months to 3 to 4 years. Comparative studies with other antiarrhythmic drugs have not been undertaken apart from a small study in atrial flutter where acecainide was better than quinidine plus digoxin. Thus, although further clinical experience is required before the relative place of acecainide in therapy can be determined, the drug nevertheless appears to offer advantages over procainamide, particularly with respect to the reduced formation of antinuclear antibodies.

Acecainide↗