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  • 1
    Electronic Resource
    Electronic Resource
    Kinetics of disopyramide in decreased hepatic function (1986)
    Springer
    European journal of clinical pharmacology 31 (1986), S. 73-77 
    Details
    ISSN: 1432-1041
    Keywords: disopyramide ; cirrhosis ; decreased hepatic function ; elimination kinetics ; alpha1-acid glycoprotein ; ischaemic heart disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The elimination kinetics of disopyramide was studied in 9 patients with decreased hepatic function (DHF) due to histologically verified cirrhosis of the liver, and in 11 patients with ischaemic heart disease (IHD). Disopyramide 100 and 150 mg was given intravenously as a bolus to the patients with IHD and DHF, respectively, followed by a continuous infusion of disopyramide 0.3 (DHF group) and 0.4 mg · min−1 (IHD group) until steady-state was achieved. A significant (p〈0.001) positive correlation between the percentage unbound and total serum concentration of disopyramide was demonstrated in both groups. The percentage of unbound disopyramide at a total serum concentration of 5.9 µmol·l−1 was 45.5% and 19.4% in the DHF and IHD groups, respectively. A negative correlation (r=−0,751,p〈0.05, and r=−0.827,p〈0.01 in the IHD and DHF patients, respectively) between the free fraction of disopyramide and alpha1-acid glycoprotein was observed. The serum concentration of alpha1-acid glycoprotein, the major binding protein of disopyramide, was significantly lower in the patients with DHF. The clearance of unbound disopyramide and its total volume of distribution and half-life were significantly lower in the DHF patients. No difference in total elimination clearance could be demonstrated. The clinical implication of the present findings appear to be that the dosage of disopyramide should be reduced by 25% when it is given intravenously to patients with decreased hepatic function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00870990
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  • 2
    Electronic Resource
    Electronic Resource
    Atenolol inhibits the elimination of disopyramide (1985)
    Springer
    European journal of clinical pharmacology 28 (1985), S. 41-43 
    Details
    ISSN: 1432-1041
    Keywords: disopyramide ; atenolol ; pharmacokinetics ; drug interaction ; ischaemic heart disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effect of atenolol on the total elimination of disopyramide and its main dealkylated metabolite was studied in 6 patients and 3 volunteers. During administration of 50 mg atenolol b.i.d. the clearance of disopyramide decreased significantly (p〈0.02) from 1.90±0.71 (X±SD) to 1.59±0.68 ml/kg/min, while its half-life, concentration of the metabolite, and the volume of distribution remained unchanged. The reduction in the clearance of disopyramide by atenolol might contribute to the alleged pharmacodynamic interaction between disopyramide and β-blocking drugs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00635706
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Haemodynamic effects and kinetics of concomitant intravenous disopyramide and atenolol in patients with ischaemic heart disease (1986)
    Springer
    European journal of clinical pharmacology 30 (1986), S. 161-166 
    Details
    ISSN: 1432-1041
    Keywords: disopyramide ; atenolol ; pharmacodynamics ; ischaemic heart disease ; haemodynamics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The haemodynamic effects of concomitant intravenous administration of disopyramide (Norpace) and atenolol (Tenormin) were studied in a cross-over trial in 7 patients with ischaemic heart disease. Following 150 mg disopyramide i.v. the cardiac index (CI) and stroke volume index (SVI) decreased by 14% and 26%, respectively and the heart rate (HR) and preejection period index (PEPI) increased by 13% and 19%, respectively. A decrease in CI of 14% and HR of 21%, respectively were noted after intravenous administration of 7.5 mg atenolol; PEPI increased by 10% whereas SVI remained unchanged. The cardiac Index (CI) fell by 33% following the administration of both drugs. The effect on CI of the two drugs was additive. The effect of disopyramide and atenolol on HR, SVI and PEPI was not significantly modified by coadministration of the other drug. No change in blood pressure was observed after disopyramide or atenolol. A correlation (ρ) of 0.540 and 0.387 was observed between the change in PEPI and the log free and total serum concentrations of disopyramide, respectively. Combined intravenous use of the two drugs in patients with incipient or overt heart failure is not recommended, unless it is due to the arrhythmia to be treated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00614295
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  • 4
    Electronic Resource
    Electronic Resource
    The effect of quinidine on the analgesic effect of codeine (1992)
    Springer
    European journal of clinical pharmacology 42 (1992), S. 587-591 
    Details
    ISSN: 1432-1041
    Keywords: Codeine ; Quinidine ; CYP2D6 ; hypolagesia ; drug interaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary We have studied the hypoalgesic effect of codeine (100 mg) after blocking the hepatic O-demethylation of codeine to morphine via the sparteine oxygenase (CYP2D6) by quinidine (200 mg). The study was performed in 16 extensive metabolizers of sparteine, using a double-blind, randomized, four-way, cross-over design. The treatments given at 3 h intervals during the four sessions were placebo/placebo, quinidine/placebo, placebo/codeine, and quinidine/codeine. We measured pin-prick pain and pain tolerance thresholds to high energy argon laser stimuli before and 1, 2, and 3 h after codeine or placebo. After codeine and placebo, the peak plasma concentration of morphine was 6–62 (median 18) nmol·.l−1. When quinidine pre-treatment was given, no morphine could be detected (〈4 nmol·l−1) after codeine. The pin-prick pain thresholds were significantly increased after placebo/codeine, but not after quinidine/codeine compared with placebo/placebo. Both placebo/codeine and quinidine/codeine increased pain tolerance thresholds significantly. Quinidine/codeine and quinidine/placebo did not differ significantly for either pin-prick or tolerance pain thresholds. These results are compatible with local CYP2D6 mediated formation of morphine in the brain, not being blocked by quinidine. Alternatively, a hypoalgesic effect of quinidine might have confounded the results.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00265920
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    Paper (German National Licenses)
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