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At least 19 recordsLinked to original sources
PubMed1975

The Wolff-Parkinson-White syndrome: pharmacologic effects of procaine amide.

The effect of procaine amide, 10 mg. per kilogram via intravenous infusion, was studied in 13 patients with the WPW syndrome. The delta wave was eliminated by procaine amide in 10 and modified in three patients. This effect lasted between 30 minutes and 8 1/2 hours and was unrelated to the total dose administered. Anterograde A-V conduction was assessed by atrial pacing with increasing rates. More rapid atrial pacing rates with 1:1 A-V conduction were observed in patients who maintained rather than lost their delta wave during pacing. Ventriculoatrial conduction was assessed with ventricular pacing at increasing rates; ventricular conduction time was fixed regardless on the pacing rate. Procaine amide significantly prolonged V-A conduction time in six and blocked V-A conduction in one patient. In addition, A-V and V-A refractory periods were measured by the extrastimulus technique. Two types of responses were observed: (1) Type I or (2) line of identity. A-V nodal refractoriness was observed to be within the normal range. Procaine amide converted anterograde line of identity responses to Type I responses in all patients who had their delta waves eliminated. In this patient group, bypass refractoriness was shorter than A-V nodal refractoriness. Procaine amide was not observed to alter significantly normal A-V conduction as assessed by atrial pacing or A-V refractory period measurements. Furthermore, a significant disparity between the effects of procaine amide on anterograde and retrograde bypass refractoriness was observed. Tachycardias could be induced in nine of the 13 patients with a mean rate of 167.2 +/- 7.9 beats per minute; delta waves were abent during all episodes of tachycardia. Procaine amide prevented tachycardia induction in six of the none patients. Procaine amide therefore demonstrates electrophysiologic effects which would be beneficial for prevention or treatment of reciprocating tachycardias in the WPW syndrome. Moreover, procaine amide would be an ideal agent for the prevention of rapid ventricular rates in patients with the WPW syndrome and atrial fibrillation.

Adolescent↗
PubMed1975

Polymorphic acetylation of procaine amide in healthy subjects.

The acetylation of procaine amide has been studied by means of gas liquid chromatography in 33 healthy human volunteers. The acetylator phenotype was determined by measuring unchanged and acetylated sulphapyridine in urine. Slow acetylators of sulphapyridine excreted significantly less procaine amide in acetylated from in the urine than rapid acetylators (9 plus or minus 1% against 19 plus or minus 4%). Hence, it is suggested that the acetylation of procaine amide is subject to the same genetic polymorphism as that of isoniazid and some sulfonamides.

Acetylation↗
PubMed1975

Acetylation of procaine amide in man. A preliminary communication.

The metabolism of procaine amide was studied in 41 cardiac patients who had achieved steady state plasma concentrations of the drug. Acetylated procaine amide accounted for 31 +/- 12% (range 16-63%) of the overall urinary recovery of the drug and is therefore a main metabolite in man. Plasma levels of the metabolite were usually lower but sometimes exceeded those of the parent compound with variations between 1 and 15 mug/ml. The metabolite had a weaker effect than procaine amide on the maximal electrical driving velocity of isolated atrial strips from guinea pig.

Acetylation↗
PubMed1975

Subcellular and functional effects of quinidine, procaine amide, and lidocaine on rat myocardium.

Different antiarrhythmic agents such as quinidine, procaine amide, and lodocaine at 1 mM concentrations were found to depress the ability of an isolated perfused rat heart to generate contractile force. Quinidine, but not procaine amide or lidocaine, decreased calcium uptake by both mitochondrial and microsomal fractions at different concentrations of calcium. The mitochondrial phosphorylation rate, respiratory control index, and state 3 oxygen consumption, but not ADP:O ratio and state 4 oxygen consumption, were depressed by only quinidine. None of these agents had any effect on myofibrillar Mg2+-ATPase or Ca2+-stimulated ATPase activities. On the other hand, sarcolemmal Mg2+-ATPase and Ca2+-ATPase activities, but not Na+-K+-ATPase activity, were increased by all these drugs. The sarcolemmal adenylate cyclase (EC 4.6.1.1) activity was decreased by quinidine only. These results suggest some similarities and differences in the sites of action of quinidine, procaine amide, and lidocaine within the myocardium.

Adenosine Triphosphatases↗
PubMed1983

Effects of procaine amide, quinidine and ethmozin on delayed afterdepolarizations.

We studied the effects of three chemically different antiarrhythmic drugs on ouabain-induced delayed afterdepolarizations (DAD) in canine Purkinje fibers. The three drugs, ethmozin, 4.6 X 10(-6) M; procaine amide, 1.1 X 10(-4) M; and quinidine, 1.13 X 10(-6) M reduced DAD amplitude equivalently at drive cycle lengths less than 500 ms. Quinidine and procaine amide in these concentrations had no effect on the action potential characteristics except for a prolongation of action potential duration (APD) induced by procaine amide. Ethmozin reduced action potential amplitude, maximum upstroke velocity of phase 0 (Vmax), and APD measured to 50% and full repolarization (APD50 and APD100). Rate dependent changes in Vmax and maximum diastolic potential (MDP) were not exaggerated by quinidine in the ouabain intoxicated Purkinje fibers. The DAD coupling interval was increased as DAD amplitude decreased with all three drugs. Although ethmozin, procaine amide and quinidine similarly reduced DAD amplitude; procaine amide and quinidine exerted these effects in the absence of other transmembrane potential effects, whereas ethmozin did so only in concentrations that depressed the action potential as well.

Action Potentials↗
PubMed1975

Cardiorenal effects of lidocaine and procaine amide in the conscious dog.

Simultaneous measurements of hemodynamics, arterioventricular (AV) conduction, and renal functioner were obtained in conscious dogs. Catheters were implanted for the long-term measurement of central aortic, right ventricular, and pulmonary artery pressure. AV conduction was assessed following surgical implantation of multipolar electrode plaques in the area of the bundle of His, as well as on the epicardium of the right and left atria and ventricles. Renal function was assessed utilizing standard techniques. Following control measurements, lidocaine, 1 mg/kg, or procaine amide, 10 mg/kg, was administered intravenously. Subsequently, serial measurements were obtained for a 90-min period. No significant changes in hemodynamics were observed following either drug. Procaine amide produced a significant increase in heart rate and a minimal increase in QRS duration associated with a decrease in low right atrial to His bundle conduction time. However, no significant changes in cardiac conduction were observed after lidocaine administration. Renal function was unaffected by lidocaine but significantly depressed by procaine amide, as demonstrated by a decrease in GFR and effective renal flow. In summary, acute administration of procaine amide significantly alters renal function in the conscious dog with minimal effects on AV conduction and hemodynamics.

Aminohippuric Acids↗
PubMed1981

Effect of procaine amide on the membrane currents of the sino-atrial node cells of rabbits.

Using small rabbit sino-atrial node preparations, the effects of procaine amide in concentrations from 0.01 to 2 mg/ml on the membrane potentials currents were studied by both current-clamp and voltage-clamp experiments. Procaine amide in concentrations over 0.1 mg/ml reduced the peak of the action potential, maximum diastolic potential and the maximum rate of depolarization. The action potential duration was prolonged, the resting potential was decreased and the heart rate was reduced. In the voltage-clamp experiments, procaine amide (0.1 mg/ml) reduced the slow inward current (is), the outward current (iK) and the inward current activated by hyperpolarization (ih). The major effect, however, was the reduction of the outward current. Sine the degree of the steady-state activation of iK and its time constant were unchanged, the observed reduction of iK could have been caused by a reduction of iK.

Action Potentials↗
PubMed1976

[Effect of prajmalium bitartrate and procaine amide on ventricular extrasystoles (author's transl)].

Prajmalium bitartrate (Neo-Gilurytmal) was given to 19 patients, who had either runs of ventricular extrasystoles or frequent extrasystoles. The E. C. G. was continuously monitored on magnetic tape. At a dosage of 80 mg/d (20 mg every six hours) a significant reduction in ventricular extrasystoles was demonstrated on 20 separate occasions. After two hours extrasystoles decreased to 63% of the initial level. After six hours practically the full effect of the drug had been reached; the reduction in extrasystoles stabilized after 12 hours at an average of 30% of initial level. Ten hours after the last tablet had been taken the frequency of extrasystoles had risen to 57% of initial level. Comparison with procaine amide (3 g/d) in 14 patients revealed no significant difference between the two drugs. Prajmalium bitartrate was well tolerated, while three patients receiving procaine amide complained of nausea and gastrointestinal symptoms, so that treatment had to be discontinued in two. In one patient, receiving procaine amide by continuous drip, there were reversible joint pains, resembling lupus erythematodes.

Adult↗
PubMed1953

PROCAINE amide.

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Procainamide↗
PubMed1978

Carrier-mediated transport of the organic cation procaine amide ethobromide by isolated rat liver parenchymal cells.

Using hepatocytes isolated by collagenase perfusion, we studied the kinetic characteristics of the uptake process for procaine amide ethobromide (PAEB). Determination of initial uptake velocities (Vo) at substrate concentrations from 30 to 400 micrometer demonstrated a saturable process with a Km of 54 +/- 10 micrometer and a Vmax of 0.13 +/- 0.01 nmol/min/mg of protein. Pretreatment of cells with metabolic inhibitors and reduction of the incubation temperature significantly reduced the Vo of 100 micrometer PAEB. Replacement of sodium ions with lithium had no effect, while replacement with choline decreased Vo by 75%. The intracellular concentration of PAEB was 18 times the medium concentration after 90 min, but 33% of that was in the acetylated form. Uptake of N4-acetyl PAEB occurred at a much lower rate and reached a cell/medium ratio of only 6 after 90 min. Only one of seven quaternary amines tested inhibited PAEB uptake at an inhibitor/substrate ratio (I/S) of 7.5, while four out of five tertiary amines significantly decreased Vo at an I/S of 0.75 and all five decreased it at a ratio of 7.5. Some organic acids and steroidal compounds also significantly decreased PAEB Vo at an I/S of 0.75, while others from each group had no effect at an I/S of 7.5. Because uptake is saturable, requires metabolic energy, and occurs against an electrochemical gradient, it is suggested that the hepatic accumulation of PAEB occurs via an active, carrier-medicated transport process.

Animals↗
PubMed1976

The effect of procaine amide on components of excitability in long mammalian cardiac Purkinje fibers.

The microelectrode technique of intracellular constant current application and intracellular transmembrane voltage recording was used to study the effects of procaine amide (PA) on cardiac excitability. We measured the effect of PA in a concentration equivalent to clinically effective antiarrhythmic plasma levels (5 mug/ml), on nonnormalized and normalized strength-duration and charge-duration curves, membrane characteristics, and cable properties in long sheep Purkinje fibers in normal Tyrode's solution with [K+]0 = 4.0 mM. PA exerted a complex action and influenced passive resistance-capacitance (RC) and active generator properties by decreasing membrane conductance, primarily membrane sodium conductance. Whether PA increased or decreased excitability depended on the relative contribution of the drug-induced alterations in passive and active membrane properties. These findings may explain, in part, the conflicting results of studies on cardiac excitability in the whole animal, as well as the clinical observation that PA may exert both artiarrhythmic and arrhythmogenic effects. The primary mechanism by which PA modifies excitability would seem to differ considerably from that of the structurally similar local anesthetic agent lidocaine.

Animals↗
PubMed1975

Effects of long-term treatment with procaine amide. A prospective study with special regard to ANF and SLE in fast and slow acetylators.

During 1970-75 a total of 42 patients have been subjected to long-term treatment with procaine amide (PrA) because of different cardiac arrhythmias and have been observed up to over 5 years. Among these patients 35 (83%) developed a significantly increased titer of ANF and of these, 12 patients (29%) developed a "classical" drug-induced SLE syndrome. In the SLE group all but 2 improved rapidly after cessation of PrA, and the ANF titer decreased continuously but slowly in both groups. Acetylation test with sulphamidine and/or isoniazid in 11 patients among the SLE cases showed 8 slow and 3 fast acetylators. Among 12 patients who also had received PrA for a long time, but had not shown any signs of an SLE syndrome, there were 10 fast and 2 slow acetylators.

Acetylation↗