Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Disopyramide”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources
PubMed1993

[Accumulation of a disopyramide metabolite in renal failure].

Twenty-nine cases of hypoglycemia induced by disopyramide (DP) have been reported in the literature to date. Twenty of the reported cases showed hypo-renal function and a high concentration was rare. DP is metabolized to mono-N-dealkyldisopyramide (MND) in the liver and accumulation of MND is to be expected in renal failure. Both DP and MND bind mainly to alpha-1-acid glycoprotein (AAG) in the plasma. In 10 hemodialysis (HD) patients with normal liver function receiving DP therapy in the steady state. DP, MND and AAG were measured pre- and post-HD. Ten patients with normal renal and liver function were selected as the controls. The DP concentration was 2.08 +/- 0.39 micrograms/ml (mean +/- SD) in the control group, and the pre- and post-HD levels were 2.40 +/- 1.08 micrograms/ml and 1.73 +/- 0.87 micrograms/ml, respectively, in the HD group. The MND concentration was 0.42 +/- 0.23 micrograms/ml in the controls, 1.53 +/- 0.52 micrograms/ml in pre-HD and 1.08 +/- 0.32 micrograms/ml in post-HD. Although DP and MND are both classified as substances of small molecular weight, the average decrease in plasma concentration from pre- to post-HD was under 30% with both agents. The MND/DP ratio in the HD group was higher than in the controls, but there was no significant difference between pre- and post-HD. The AAG level was 75 +/- 5mg/dl in the controls and 109 +/- 11mg/dl before HD in the HD group (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Accumulation of a disopyramide metabolite in renal failure.

Ten hemodialysis (HD) patients with normal liver function received disopyramide (DP) therapy in the steady state. DP, mono-N-dealkyldisopyramide (MND) and alpha-1-acid glycoprotein (AAG) were measured before and after HD. Ten patients with normal renal and liver function were selected as controls. The DP concentration was 2.08 +/- 0.39 micrograms/ml (mean +/- SD) in the control group, and the pre and post HD levels were 2.40 +/- 1.08 micrograms/ml and 1.73 +/- 0.87 micrograms/ml, respectively, in the HD group. The MND concentration was 0.42 +/- 0.23 microgram/ml in controls, 1.53 +/- 0.52 micrograms/ml in pre HD and 1.08 +/- 0.32 microgram/ml in post-HD. Although DP and MND are both classified as small molecular weight substances, the average decrease in plasma concentration from pre to post HD was under 30% with both agents. The MND/DP ratio in the HD group was higher than in controls, but there was no significant difference between pre and post HD. The AAG level was 75 +/- 5 mg/dl in controls and 109 +/- 11 mg/dL before HD in the HD group (p < 0.001). In conclusion, an MND accumulation was observed in HD patients receiving DP therapy. Because the anticholinergic effect of MND is 24 times that of DP, MND is thought to contribute in some way to the hypoglycemia induced by DP in renal failure.

Adult↗
PubMed1993

Prolonged cardiopulmonary resuscitation during acute disopyramide poisoning.

A case is reported of sustained electromechanical dissociation due to deliberate disopyramide over-dosage in a young healthy girl. Circulatory recovery was achieved with standard resuscitative measures, including prolonged cardiac massage and isoproterenol infusion plus high dose calcium chloride. Neurological recovery was complete.

Acute Disease↗
PubMed1993

A potent inhibitory effect of erythromycin and other macrolide antibiotics on the mono-N-dealkylation metabolism of disopyramide with human liver microsomes.

Clinical observation has suggested that erythromycin (EM) may cause an elevation in plasma disopyramide (DP) concentrations and thereby cause potentially fatal arrhythmias in certain patients. To determine whether EM would interfere with the in vivo pharmacokinetics of DP and whether other macrolides would share this action with EM, the effects of EM and other macrolide antibiotics on the in vitro DP metabolism to its major metabolite, mono-N-dealkyldisopyramide, were studied with human liver microsomes obtained from eight patients who underwent partial hepatectomy. The mono-N-dealkylation of DP proceeded with a biphasic enzyme kinetic profile, suggesting that at least two distinct enzyme sites or components are involved in the DP metabolism in humans. The high- and low-affinity sites gave the mean (+/- S.D.) Km of 5.7 +/- 2.8 and 724.7 +/- 427.4 microM, and Vmax of 2.90 +/- 1.17 and 18.20 +/- 8.84 nmol/hr/mg protein, respectively. Because the mean intrinsic clearance (i.e., Vmax/Km) for the high-affinity site (i.e., 0.79 +/- 0.69 ml/hr/mg protein) was about 30 times greater than that for the low-affinity site (i.e., 0.03 +/- 0.01 ml/hr/mg protein), the high-affinity site was considered more important in the DP metabolism at its therapeutic concentrations (i.e., 2-5 micrograms/ml or 5-14 microM). EM inhibited the high-affinity site activity in a noncompetitive manner with the mean Ki of 19.5 +/- 1.3 microM (n = 4). An EM concentration associated with a 50% suppression of the DP metabolism at 30 microM (i.e., IC50) was 94 microM.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMedDate not supplied

Oral disopyramide in the treatment of recurrent neurocardiogenic syncope.

In neurocardiogenic syncope the normal compensatory response on assuming an upright posture is interrupted after several minutes and replaced by a paradoxical withdrawal of sympathetic activity and increased parasympathetic activity. The resulting reduction in blood pressure is severe, sympathetic activity is inhibited, plasma norepinephrine levels do not increase and the heart rate decreases. The defect is a paradoxical interruption of sympathetic excitation associated with parasympathetic excitation, causing profound vasodilatation and bradycardia. Disopyramide has been shown not only to treat the bradycardia but also to control the hypotension.

Aged↗
PubMedDate not supplied

Isotachophoretic determination of bisoprolol, clonidine, disopyramide and tolazoline in human fluids.

Separation and determination of bisoprolol, clonidine, disopyramide and tolazoline in control serum and in human urine was investigated by capillary isotachophoresis. The drugs were separated by using the cationic electrolyte system. viz., sodium acetate buffer (pH 4.64) (c1 = 10 mM)-beta-alanine. The compounds were almost totally isolated from serum by solid-phase extraction using a Sep-Pak C18 cartridge. The recovery of compounds varied from 87 to 99%. The linear calibration range was studied to apply the method to real human fluids. The limit of determination of the drugs was 40.0 micrograms/ml serum. The limit of determination by direct sampling for bisoprolol is 3 micrograms/ml urine.

Adrenergic alpha-Agonists↗
PubMed1976

[Disopyramide phosphate: electrophysiological and inotropic effects in isolated cat papillary muscles and comparison with quinidine (author's transl)].

The effects of 4-diisopropylamino-2-phenyl-2-(2-pyridyl)-butyramide monophosphate (disopyramide phosphate; D; 10(-6)--10(-4) M) on transmembrane resting potential, action potential, effective refractory period and twitch tension were simultaneously studied in electrically driven (frequency 1 Hz) papillary muscles isolated from the right ventricles of cats. The experiments were performed at 35degrees C with intracellular glass microelectrodes. Quinidine sulfate (10(-6)--10(-4) M) was used for comparison. D increased the duration of the action potential during phase 3 (90% repolarization) in a concentration-dependent manner. The effective refractory period was prolonged by nearly the same extent whereas the maximal rate of rise of the action potential was reduced. The overshoot was slightly decreased only at 10(-4) M. Resting potential and plateau phase of the action potential were not affected by D. The effects of D on the electrical events were accompanied by concomitant decreases in twitch tension. The effects of quinidine were essentially similar to those obtained with D. It is concluded that the effects of D on dV/dtmax and effective refractory period observed in cat papillary muscle may account for the clinically observed efficacy of D to overcome ventricular arrhythmias. The results suggest also that the mechanism of the ventricular effects of D is similar to that of quinidine.

Action Potentials↗
PubMed1988

Activation block and trapping of penticainide, a disopyramide analogue, in the Na+ channel of rabbit cardiac Purkinje fibers.

The blocking mechanism of the Na+ channel by penticainide, a disopyramide analogue, was studied in rabbit cardiac Purkinje fibers. Na+ channel activity was measured directly by recording the slowly inactivating Na+ current or indirectly by measuring Vmax. The two-microelectrode technique was used to measure currents under voltage-clamp conditions or to impose different degrees and durations of depolarizing pulses. The experimental results show 1) that penticainide exerted a pronounced use-dependent block not dependent on the duration of the depolarizing pulse, 2) that no block was observed in the absence of stimulation, even when the membrane was depolarized by conditioning prepulses, and 3) that recovery was slower the more negative the holding potential but could be accelerated by repeating the depolarizing pulse; there was not only use-dependent block but also use-dependent unblock. It is concluded that penticainide binds to the open Na+ channel and is trapped when the activated channel returns to the rested state.

Action Potentials↗
PubMed2006

CE coupling with end-column electrochemiluminescence detection for chiral separation of disopyramide.

CE with electrochemiluminescence (ECL) detection technique was successfully applied for the chiral separation of a kind of class IA antiarrhythmic racemic drug. To the best of our knowledge, this is the first report of ECL detection used in chiral CE. To get better detection sensitivity and good enantioresolution at the same time, the conditions of capillary inlet and outlet buffer were systematically optimized. Unlike the traditional chiral separation method, the buffers we used in the capillary inlet and outlet differed from each other in terms of buffer pH, ionic strength, type of BGE as well as buffer composition. Under the optimum conditions, baseline enantioseparation and highly sensitive detection of the enantiomers were achieved. Wide linear relationship of each enantiomer was achieved in the range of 5 x 10(-7) to 2 x 10(-5) mol/L with relative coefficients of 0.996 and 0.997, respectively. The detection limits were estimated to be 8 x 10(-8) and 1.0 x 10(-7) mol/L (S/N = 3) for the enantiomers, respectively. In addition, a successful application of this new method to the chiral separation of the racemic drug in spiked plasma samples confirmed the validity and applicability of the chiral CE-ECL method.

Anti-Arrhythmia Agents↗