The effect of the dextro isomer of propranolol on sinus rate and cardiac arrhythmias

Howitt, G.; Husaini, M; Rowlands, Dewi K.; Logan, W.F.W.E.; Shanks, R. G.; Evans, M.

doi:10.1016/0002-8703(68)90258-5

Cited by 27 publications

(5 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the isolated rat heart, d-propranolol was as effective as racemic beta-adrenergic antagonists in preventing arrhythmias after coronary occlusion (33) and subsequent reperfusion (34). In small groups of patients, there have been anecdotal reports ihat d-propranolol can suppress premature atrial and ventricular depolarizations (35,36). However, none of these investigations explored the mechanism of its antiarrhythmic actions.…”

Section: Discussionmentioning

confidence: 99%

Suppression of ventricular arrhythmias in man by d-propranolol independent of beta-adrenergic receptor blockade.

Murray¹,

Reilly²,

Koshakji³

et al. 1990

J. Clin. Invest.

View full text Add to dashboard Cite

To investigate the mechanisms of ventricular arrhythmia suppression by propranolol, we determined the antiarrhythmic efficacy of d-propranolol in 10 patients with frequent ventricular ectopic depolarizations (VEDs) and nonsustained ventricular tachycardia. After an initial placebo phase, 40 mg d-propranolol was administered orally every 6 h with dosage increased every 2 d until arrhythmia suppression (> 80% VED reduction), intolerable side effects, or a maximal dosage (1,280 mg/d) was reached. Response was verified by documenting return of arrhythmia during a final placebo phase. Arrhythmia suppression occurred in six patients while two more had partial responses. Effective dosages were 320-1,280 mg/d (mean 920±360, SD) of d-propranolol with corresponding plasma concentrations of 60-2,280 ng/ml (mean 858±681). For the entire group, the QTc interval shortened by 4±4% (P = 0.03). Arrhythmia suppression was accompanied by a reduction in peak heart rate during exercise of 0-29%. To determine whether arrhythmia suppression could be attributed to betablockade, racemic propranolol was then administered in dosages producing the same or greater depression of exercise heart rate. In 3/8 patients, arrhythmias were not suppressed by racemic propranolol indicating that d-propranolol was effective via a non-beta-mediated action. By contrast, in 5/8 patients racemic propranolol also suppressed VEDs. We conclude that propranolol suppresses ventricular arrhythmias by both beta-and non-beta-adrenergic receptor-mediated effects. (J. Clin. Invest. 1990.85:836-842.) propranolol * antiarrhythmic * ventricular arrhythmias * dextropropranolol-betaadrenergic receptor blockade

show abstract

Section: Discussionmentioning

confidence: 99%

Suppression of ventricular arrhythmias in man by d-propranolol independent of beta-adrenergic receptor blockade.

Murray¹,

Reilly²,

Koshakji³

et al. 1990

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…In view of its effects in controlling dysrhythmias in animals and patients undergoing anaesthesia (Howitt et al, 1968), it seems possible that this isomer will prove as effective as the DL mixture and certainly justifies further clinical trial. We gave it in larger doses and with less myocardial depression than racemic propranolol to 13 patients with recent myocardial infarction.…”

Section: Discussionmentioning

confidence: 99%

“…D-Propranolol possesses considerable antidysr&hythmic activity and will rapidly revert ouabain-induced tachycardia in dogs and cats to sinus rhythm (Howe and Shanks, 1966). Howitt was able to control various dysrhythmias in 59 patients (Howitt, Husaini, Rowlands, Logan, Shanks, and Evans, 1968) and reported that 5-20 mg. of dextropropranolol given intravenously was as effective as the racemic drug in treating ventricular and supraventricular ectopic beats. In six of his patients the dextro-isomer terminated digitalisinduced dysrhythmias.…”

mentioning

confidence: 99%

Haemodynamic effects of dextro-propranolol in acute myocardial infarction

Baldry¹,

Balcon²,

Hoy³

et al. 1970

Thorax

View full text Add to dashboard Cite

“…In the use of propranolol in this arrhythmia, it appears that the direct membrane action is responsible for reversion to sinus mechansim and the beta-blocking action reduces nodal conduction. 29 , 41 Since it is well established that fatal ventricular arrhythmias can follow the use of direct-culTent countershock in the presence of excessive or even normal amounts of digitalis,44 the use of propranolol, diphenylhydantoin, or lidocaine is superior to electrical conversion in patients with sustained supraventricular or ventricular tachycardias which might be caused by digitalis.…”

Section: Clinical Pharmacology and Therapeuticsmentioning

confidence: 99%

The clinical pharmacology and therapeutic applications of the antiarrhythmic drugs

Mason

Spann

Zelis

et al. 1970

Clin Pharma and Therapeutics

View full text Add to dashboard Cite

The mechanisms of action and therapeutic applications of the commonly employed and new antiarrhythmic agents are best understood by consideration of the basic electrophysiologic properties of heart muscle affected by these drugs. Thus, each of these agents depresses disorders of impulse formation by reducing diastolic depolarization and thereby diminishing automaticity and inhibits disorders of impulse conduction by altering conduction velocity and refractory period and thereby disrupting re-entry mechanisms. Accompanying these antiarrhythmic actions, quinidine, procaine amide (Pronestyl), propranolol (Inderal), and potassium worsen atrioventricular block; whereas lidocaine (Xylocaine) usually does not influence nodal conduction velocity, and diphenylhydantoin accelerates this property in the atrioventricular node. Quinidine and procaine amide directly prolong refractory period; in contrast, lidocaine, diphenylhydantOin, and proprarwlol directly reduce this period. Quinidine and procaine amide are useful in most types of supraventricular and ventricular tachyarrhythmias. Propranolol is particularly effective against supraventricular arrhythmias; however, lidocaine is only moderately effective in disorders of atrial rhythm but markedly suppresses ventricular tachyarrhythmias. Diphenylhydantoin (Dilantin) and bretylium (Darenthin) are most beneficial in terminating disorders of ventricular rhythm and, in the case of bretylium, particularly those due to re-entry mechanisms. Diphenylhydantoin, propranolol, and lidocaine possess electrophysiologic properties that are particularly salutary in the treatment of digitalis toxicity. In general, antiarrhythmic agents have depressant effects on cardiac contractility which are related to dose, speed of administration, and extent of myocardial disease.In con/'rast, bretylium possesses positive inotropic actions, and potassium within normal serum concentrations has no effect on contractile state. It is suggested that the fundamental subcellular actions of antiarrhythmic agents occur as a consequence of their binding to the cell membrane; in this manner, altered transmembrane fluxes of sodium and potassium ions underlie the electrophysiologic effects, and those of calcium ions underUe the contractile properties of these agents. From these observations, the thorough understanding of basic and applied pharmacology of the antiarrhythmic agents prOVides for their more iudicious use in patients.

show abstract

The effect of the dextro isomer of propranolol on sinus rate and cardiac arrhythmias

Cited by 27 publications

References 11 publications

Suppression of ventricular arrhythmias in man by d-propranolol independent of beta-adrenergic receptor blockade.

Suppression of ventricular arrhythmias in man by d-propranolol independent of beta-adrenergic receptor blockade.

Haemodynamic effects of dextro-propranolol in acute myocardial infarction

The clinical pharmacology and therapeutic applications of the antiarrhythmic drugs

Contact Info

Product

Resources

About