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Biomedical subjects

B D Christiansen

Publications and source records attributed to B D Christiansen.

7 recordsLinked to original sources
PubMed1992

[Angina pectoris after sumatriptan (Imigran)].

Developed for the treatment of migraine, sumatriptan is an agonist of 5-hydroxytryptamine-1-receptors. Though a pressure sensation is a common complaint, significant ECG changes have not been reported after subcutaneous administration of sumatriptan. A case history is given where angina pectoris after sumatriptan self-administration was experienced on two occasions by a 61-year old man with a history of minor myocardial infarction--without post-infarction angina--two years previously. The angina after sumatriptan was accompanied on both occasions by significant ST-segment depression on ECG-monitoring. An extracranial vasoconstrictor action of sumatriptan in patients with ischaemic heart disease is suggested.

Angina Pectoris↗
PubMed1983

Influence of verapamil on the inotropism and pharmacokinetics of digoxin.

Verapamil has been demonstrated to inhibit the elimination of digoxin and to increase its steady state plasma level by 60-80%. Animal studies suggest that verapamil abolishes the intropic action of other drugs such as ouabain and dopamine. The clinical consequences of this drug interaction were investigated by examining the inotropic activity of single doses of digoxin (assessed from systolic time intervals), with and without coadministration of verapamil. Verapamil decreased total-body clearance of digoxin from 4.68 +/- 0.41 to 3.29 +/- 0.26 ml/min/kg (p less than 0.001) and increased the plasma half-life of the drug from 33.50 +/- 2.38 to 41.31 +/- 2.27 h (p less than 0.01). Verapamil had no influence on the base-line values of the systolic time intervals. Both in the absence and presence of verapamil, digoxin caused significant shortening of the total electromechanical systole and the left ventricular ejection time. However, compared to control conditions, the decay of these changes was slower in the presence of verapamil, in parallel with the prolongation of the plasma half-life of digoxin. A linear relationship was established between reductions in the systolic time intervals and the computer-derived concentration of digoxin in the deep compartment. These regression lines, which represent the concentration-effect relationships of the inotropism of digoxin, were not affected by verapamil. Thus, verapamil per se had no measurable effect either on base-line contractile function of the heart or on digoxin-induced inotropism. The elevated plasma digoxin concentration induced by verapamil appears cardioactive in terms of inotropism.

Adult↗
PubMed1983

Effect of quinidine on digoxin bioavailability.

To evaluate the possible effect of quinidine on digoxin bioavailability, the steady state digoxin kinetics was examined with and without concomitant quinidine therapy, in 7 cardiac patients after simultaneous administration of oral digoxin and intravenous [3H]-digoxin. In the presence of quinidine, the absorption rate constant of digoxin (ka) increased from 2.72 +/- 1.04 to 3.53 +/- 1.34 h-1 (p less than 0.05), whereas lag time and peak time decreased from 0.16 +/- 0.10 to 0.05 +/- 0.04 h (p less than 0.05) and from 0.92 +/- 0.27 to 0.69 +/- 0.19 h (p less than 0.02), respectively. Predose plasma digoxin increased from 0.41 +/- 0.25 to 0.70 +/- 0.31 ng/ml (p less than 0.02), while peak plasma digoxin increased from 0.93 +/- 0.34 to 1.63 +/- 0.46 ng/ml (p less than 0.02). The systemic availability of digoxin increased from 68.48 +/- 13.35 to 79.09 +/- 14.89% (p less than 0.05) in the presence of quinidine. Quinidine had no effect on the biotransformation pattern of digoxin, as assessed by thin layer chromatography. Quinidine increases the rate and extent of digoxin absorption, and this interaction contributes significantly to the elevation in plasma digoxin during both its distribution and elimination phases.

Aged↗
PubMed1983

Verapamil-induced changes in digoxin kinetics and intraerythrocytic sodium concentration.

Verapamil increases plasma digoxin concentration by about 60% to 80%. To explore the clinical consequences of this interaction, we evaluated single-dose digoxin kinetics along with repeated measurements of intraerythrocytic sodium concentration in eight healthy subjects before and during verapamil coadministration. Verapamil reduced mean total body clearance of digoxin from 4.68 +/- 0.41 to 3.29 +/- 0.26 ml/min/kg and prolonged digoxin biologic t1/2 from 33.5 +/- 2.4 to 41.4 +/- 2.3 hr. These kinetic changes were associated with a greater elevation of intraerythrocytic sodium concentration than controls. Verapamil had no effect on intraerythrocytic sodium content. In vitro experiments revealed no influence of verapamil on the number of glycoside receptors on human lymphocytes. Since intracellular sodium concentration has proved to correlate closely with clinical signs of digoxin toxicity, our indicate that verapamil is likely to increase the risk of digoxin-induced arrhythmias.

Adult↗
PubMed1983

Changes in steady state digoxin pharmacokinetics during quinidine therapy in cardiac patients: influence of plasma quinidine concentration.

In seven cardiac patients on long-term digoxin therapy, digoxin kinetics were investigated - in the absence and presence of quinidine - after simultaneous administration of an oral digoxin dose and an intravenous 3H-digoxin bolus injection. From 3H-digoxin data quinidine was found to decrease both renal (from 1.19 +/- 0.35 to 0.86 +/- 0.21 ml/min./kg) (P less than 0.02) and extrarenal clearances of digoxin (from 0.85 +/- 0.24 to 0.49 +/- 0.23 ml/min./kg) (P less than 0.02), and to diminish the steady state distribution volume of the drug (from 6.78 +/- 1.23 to 5.63 +/- 1.64 l/kg) (P less than 0.02). Plasma half-life increased from 51.5 +/- 5.4 to 64.4 +/- 14.8 hrs (P less than 0.05), while urinary excretion half-life increased from 54.4 +/- 3.9 to 78.5 +/- 14.1 hrs (P less than 0.01). Pharmacokinetic parameters derived from plasma and urinary digoxin data showed similar changes during quinidine therapy. Reduction in renal 3H-digoxin clearance occurred at subtherapeutic plasma quinidine levels and was independent of plasma quinidine, whereas reductions in extrarenal 3H-digoxin clearance and 3H-digoxin distribution volume were positively correlated to plasma quinidine concentrations (P less than 0.05).

Creatinine↗