Cardiopulmonary effects of antimalarial drugs
Identifieur interne : 003B97 ( Main/Exploration ); précédent : 003B96; suivant : 003B98Cardiopulmonary effects of antimalarial drugs
Auteurs : Shigeru Matsuo [États-Unis] ; Ruy Ruiz [États-Unis] ; James Smith Jr. [États-Unis] ; Domingo M. Aviado [États-Unis]Source :
- Toxicology and Applied Pharmacology [ 0041-008X ] ; 1970.
English descriptors
- Teeft :
- Action potentials, Anesthetized, Anesthetized dogs, Anesthetized rabbits, Antiarrhythmic, Antimalarial, Antimalarial drugs, Aortic, Aortic blood flow, Arterial blood pressure, Atria1, Atria1 muscle, Atria1 rate, Aviado, Cardiac, Cardiac effects, Cardiac output, Catecholamine, Contractile force, Control injection, Cycle length, Depolarization, Depolarization time, Diaminopyrimidines, Folic, Folic acid, Folk acid, Further prolongation, Heart rate, Infusion, Inhalation, Next group, Organ bath, Pharmacol, Pretreatment, Prolongation, Pulmonary resistance, Pyrimethamine, Rats pretreated, Repolarization, Repolarization time, Reserpine, Subcutaneously, Transmembrane, Trimethoprim, Ventricular, Ventricular function.
Abstract
Abstract: WR 40,070 (5-piperonyl-2-4-diaminopyrimidines) was compared with trimethoprim in 4 animal species: mice, rats, rabbits, and dogs. The most important difference between the two compounds uncovered in our investigation is the nature of their cardiac effects. Trimethoprim caused a decrease in cardiac output in the anesthetized dogs whereas WR 40,070 caused an increase. The mechanism responsible for the difference was demonstrated in the dog heart-lung preparation. WR 40,070 caused an improvement in ventricular function by releasing catecholamines. The heart-lung prepared from a dog previously treated with reserpine did not show the cardiac stimulation characteristic of WR 40,070. The transmembrane potential recorded from the isolated rat atrial muscle revealed some changes which suggest that the anti-folic acid activity of this compound and pyrimethamine cause prolongation of repolarization time. The in vitro addition of folic acid caused further prolongation of repolarization time. These changes are not related to the primary changes in contractility and excitability brought about by diaminopyrimidines.
Url:
DOI: 10.1016/0041-008X(70)90138-9
Affiliations:
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Le document en format XML
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<term>Anesthetized rabbits</term>
<term>Antiarrhythmic</term>
<term>Antimalarial</term>
<term>Antimalarial drugs</term>
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<term>Aortic blood flow</term>
<term>Arterial blood pressure</term>
<term>Atria1</term>
<term>Atria1 muscle</term>
<term>Atria1 rate</term>
<term>Aviado</term>
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<term>Cardiac effects</term>
<term>Cardiac output</term>
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<term>Contractile force</term>
<term>Control injection</term>
<term>Cycle length</term>
<term>Depolarization</term>
<term>Depolarization time</term>
<term>Diaminopyrimidines</term>
<term>Folic</term>
<term>Folic acid</term>
<term>Folk acid</term>
<term>Further prolongation</term>
<term>Heart rate</term>
<term>Infusion</term>
<term>Inhalation</term>
<term>Next group</term>
<term>Organ bath</term>
<term>Pharmacol</term>
<term>Pretreatment</term>
<term>Prolongation</term>
<term>Pulmonary resistance</term>
<term>Pyrimethamine</term>
<term>Rats pretreated</term>
<term>Repolarization</term>
<term>Repolarization time</term>
<term>Reserpine</term>
<term>Subcutaneously</term>
<term>Transmembrane</term>
<term>Trimethoprim</term>
<term>Ventricular</term>
<term>Ventricular function</term>
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<front><div type="abstract" xml:lang="en">Abstract: WR 40,070 (5-piperonyl-2-4-diaminopyrimidines) was compared with trimethoprim in 4 animal species: mice, rats, rabbits, and dogs. The most important difference between the two compounds uncovered in our investigation is the nature of their cardiac effects. Trimethoprim caused a decrease in cardiac output in the anesthetized dogs whereas WR 40,070 caused an increase. The mechanism responsible for the difference was demonstrated in the dog heart-lung preparation. WR 40,070 caused an improvement in ventricular function by releasing catecholamines. The heart-lung prepared from a dog previously treated with reserpine did not show the cardiac stimulation characteristic of WR 40,070. The transmembrane potential recorded from the isolated rat atrial muscle revealed some changes which suggest that the anti-folic acid activity of this compound and pyrimethamine cause prolongation of repolarization time. The in vitro addition of folic acid caused further prolongation of repolarization time. These changes are not related to the primary changes in contractility and excitability brought about by diaminopyrimidines.</div>
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<name sortKey="Smith Jr, James" sort="Smith Jr, James" uniqKey="Smith Jr J" first="James" last="Smith Jr.">James Smith Jr.</name>
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