Why the study?
Do beta adrenergic blocking agents (pronethalol and INPEA) inhibit induced arrhythmias in a preclinical model?
Do beta adrenergic blocking agents (pronethalol and INPEA) inhibit induced arrhythmias in a preclinical model?
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Early preclinical evidence demonstrating that beta-blockers inhibit sympathomimetic-induced arrhythmias via specific adrenergic blockade, with pronethalol exhibiting additional quinidine-like antiarrhythmic properties.
Pronethalol and N-isopropyl- p -nitrophenyl-ethanolamine (INPEA) were found to antagonize the inotropic and chronotropic actions of epinephrine and isoproterenol as well as the vasodilator action of the latter, thus confirming the beta adrenergic blocking actions of the two agents. The two agents also antagonized the cardiac arrihythmias induced by epinephrine but not those produced by coronary artery ligation. The ventricular tachycardia produced by ouabain was suppressed by pronethalol but not by INPEA. A parallelism between beta adrenergic blockade produced by pronethalol and its antiarrhythmic act ion against epinephrine but not against ouabain was observed. The beta adrenergic blocking agents thus appear to inhibit arrlmythmias induced by sympathomimetic amines on the basis of specific adrenergic blockade. On the other hand, pronethalol suppressed the ouabain-induced arrhythmia apparently because of an additional nonspecific ( quinidinelike) action.
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Somani et al. (1965) studied this question.
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