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Side 1 fra 142 resultater
Problems in assessing infarction size by epicardial mapping: preliminary studies with quinidine.
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Some of the laboratory difficulties in assessing infarction size produced by intermittent coronary artery occlusion were demonstrated by using an epicardial mapping technique in anesthetized open-chest dogs. Intermittent occlusion of a left anterior descending coronary artery branch resulted in a
Hemodynamic effects of procainamide and quinidine and the influence of beta-blockade before and after experimental myocardial infarction.
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The use of antiarrhythmie drugs in combination has been limited because of possible side effects secondary to myocardial depression in the acute myocardial infarction patient. Therefore, we investigated in intact dogs (group I) the hemodynamic interaction of propranolol plus procainamide (subgroup
Steady-state serum quinidine concentration: role in prophylactic therapy following acute myocardial infarction.
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Steady-state serum quinidine concentrations were monitored in 24 patients with acute myocardial infarction who were on a 1,300-mg daily dosing regimen. Mean serum concentrations spanned the therapeutic range, from 2 to 6 microgram/ml in 21 patients. In no patient was the level of 7 microgram/ml
Altered therapeutic range for quinidine after myocardial infarction and cardiac surgery.
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Although most assays for measuring drug levels in serum determine the total concentration, effects from a drug are determined better by measuring the concentration of unbound (free) drug in serum. When the free fraction of a drug is constant, the total drug concentration may act as a good guide in
Characteristics of I(K) and its response to quinidine in experimental healed myocardial infarction.
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BACKGROUND
Mechanisms and drug treatment of serious ventricular arrhythmias in patients with healed myocardial infarction (HMI) are incompletely understood, in part because the electrophysiology and pharmacology of myocytes from noninfarcted regions of HMI hearts are not well
Epicardial activation patterns of torsade de pointes in canine hearts with quinidine-induced long QT interval but without myocardial infarction.
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We studied the epicardial activation sequence during torsade de pointes in canine hearts with quinidine-induced long QT interval. Following a toxic dose of quinidine sulfate (30 mg/kg), polymorphic ventricular tachycardia was induced by extrastimuli. In nine dogs, 22 episodes of nonsustained
[Prevention of sudden death in heart infarct by means of quinidine or procaine amide].
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[On the treatment of the coronary infarct with quinidine-procaine amide].
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[Quinidine in acute heart infarct].
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Prophylactic quinidine after myocardial infarction.
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Quinidine in acute myocardial infarction.
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Quinidine lactate and gluconate in the suppression of ectopic ventricular tachycardias associated with myocardial infarction; control of toxicity by morphine.
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Effect of quinidine and tranquillising agents on ectopic ventricular tachycardia resulting from acute myocardial infarction in the dog.
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Prophylactic use of quinidine following myocardial infarction.
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THE USE OF QUINIDINE SULFATE DURING MYOCARDIAL INFARCTION.
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