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quinidine/vomissement
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Interaction between quinidine and digoxin.
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The serum digoxin concentration increased in 25 of 27 study patients (93%), and the mean serum digoxin concentration rose from 1.4 ng/ml to 3.2 ng/ml during quinidine therapy. Anorexia, nausea, or vomiting developed in 16 patients (59%) but disappeared in all ten patients for whom the digoxin dose
Clinical and electrophysiological effects of intravenous quinidine in man.
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Quinidine gluconate (total dose 4-4 to 9-1 mg/kg) was infused intravenously over 22 minutes in 20 patients with either frequent premature ventricular contractions or supraventricular arrhythmias, 16 of whom had bundle-branch block. Therapeutic plasma quinidine levels (3 to 7 mg/l) were achieved in
[Treatment of atrial fibrillation using intravenous infusion of quinidine].
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Quinidine gluconate was administered slowly by intravenous infusion to 20 patients with atrial fibrillation. Nineteen of them had rheumatic heart disease and the other one had Ebstein's disease. The first ten patients received 0.027 mg/kg/min during 6 hs or less if they returned to normal sinus
Digoxin-quinidine interaction in the dog.
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In seven healthy dogs, digoxin was given as an oral loading dose (0.05 mg/kg/day) on the first day, followed by an oral maintenance dose (0.02 mg/kg/day) during the next 14 days. On the sixth day of digoxin treatment, oral quinidine (200 mg b.i.d.) was added until the tenth day. Plasma
A previously unrecognized drug interaction between quinidine and digoxin.
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Following the development of digoxin radioimmunoassay, we noted that serum digoxin concentrations appeared to rise in patients given quinidine. To further evaluate this important possible interaction between digoxin and quinidine, charts from 863 cardiology patients were reviewed. Ninety two
The effect of quinidine and other oral antiarrhythmic drugs on serum digoxin. A prospective study.
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We compared the effects of quinidine and three alternate antiarrhythmic drugs on serum digoxin concentration in 63 patients before and during administration of quinidine, procainamide, disopyramide, or mexiletine. Quinidine increased digoxin concentration by at least 0.5 nmol/L in 21 of 22 patients:
Evaluation of the combination of vinblastine and quinidine in patients with metastatic renal cell carcinoma. A phase I study.
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Quinidine is known to inhibit p-glycoprotein and enhance the activity of vinblastine against cultured renal carcinoma cells. We have combined quinidine and vinblastine in a Phase I trial in patients with metastatic renal cell carcinoma. Twenty-three patients were entered. Prior treatment included
CYP2D6 basic genotyping as a potential tool to improve the antiemetic efficacy of ondansetron in prophylaxis of postoperative nausea and vomiting.
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BACKGROUND
Postoperative nausea and vomiting (PONV) is a common complication after anesthesia and surgery. Ondansetron is one of the most widely used drugs in the prophylaxis of PONV and is extensively metabolized in humans. In vitro metabolism studies have shown that ondansetron is a substrate for
Quinine-induced arrhythmia in a patient with severe malaria.
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It was reported that there was a case of severe malaria patient with jaundice who presented with arrhythmia (premature ventricular contraction) while getting quinine infusion was reported. A man, 25 years old, was admitted to hospital with high fever, chill, vomiting, jaundice. The patient was fully
Therapy of ventricular tachycardia.
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Therapeutic modalities for ventricular tachycardia include antiarrhythmic drugs, direct current cardioversion, electrical pacing and surgical intervention. Lidocaine, procainamide and bretylium are all capable of controlling recurrent ventricular tachycardia; bretylium has the advantage of also
Propafenone: a new antiarrhythmic agent.
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The chemical and pharmacologic properties, pharmacokinetics, drug interactions, clinical efficacy, adverse effects, and dosage of propafenone are reviewed. Propafenone is a class IC antiarrhythmic agent that is structurally similar to the beta blockers but that has only weak beta-blocking and
Intramuscular artemether in female patients with uncomplicated falciparum malaria.
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Thirty-three female patients suffering from acute uncomplicated falciparum malaria were treated with intramuscular artemether for 5 days during May-October 1990. Fourteen patients received 160 mg as an initial dose, followed by 80 mg daily for 4 days. Nineteen patients with low body weight (mean
DKA-induced Brugada phenocopy mimicking STEMI.
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UNASSIGNED
A 47-year-old Caucasian woman with type 1 diabetes presented with epigastric pain and vomiting. She had not been adherent with her diet and insulin therapy for the past 3 weeks. She never had a personal or family history of arrhythmia-related symptoms, ventricular tachycardia or
Characterization of the cytochrome P450 enzymes involved in the in vitro metabolism of dolasetron. Comparison with other indole-containing 5-HT3 antagonists.
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Dolasetron mesilate [(2 alpha, 6 alpha, 8 alpha, 9a beta)-octahydro-3-oxo-2,6-methano-2H-quinolizin-8-yl-1H-indole-3-c arboxylate monomethane-sulfonate], is a 5-HT3 receptor antagonist, which is in development for the treatment of chemotherapy-induced emesis. The compound is rapidly reduced by
[Severe poisoning with digitalis treated by the administration of anti-digoxin antibodies].
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A case report of severe digitalis poisoning in a patient with prosthetic heart valve is presented. He complained of nausea, vomiting, drowsiness, temporal disorientation and lethargy. The electrocardiogram showed idioventricular rhythm, and plasma levels of digoxin were 6.78 ng/ml. Predisposing
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