Mechanisms of Action of Antiarrhythmic Drugs

Rosen, Michael R.; Hoffman, B. F.

doi:10.1161/01.res.32.1.1

Cited by 138 publications

(29 citation statements)

References 9 publications

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“…Bretylium possesses antiadrenergic and hypotensive actions associated with depletion of norepinephrine from peripheral adrenergic nerve endings. 4 In accordance with this known mechanism, some subjects treated with bretylium may not be able to recover as well from fibrillation-defibrillation episodes because of less effective autonomic reflexes. In a clinical study, however, Haynes et al 8 found no differences in resuscitative results (short term or long term survival) for patients after use of bretylium as compared to lidocaine.…”

Section: Discussionmentioning

confidence: 99%

“…4 Bretylium, like clofilium, has been reported to produce chemical defibrillation in the absence of a defibrillator countershock. 5 Because of the apparent ability of these two agents to make defibrillation easier, and because of their unique pharmacological characteristics, the authors have investigated the effects of intravenous clofilium phosphate and bretylium tosylate on ventricular defibrillation threshold in dogs.…”

Section: Introductionmentioning

confidence: 99%

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The effect of newer antiarrhythmic drugs on defibrillation threshold

Tacker

Niebauer

Babbs

et al. 1980

Critical Care Medicine

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This study was conducted to determine the effects of clofilium phosphate and bretylium tosylate on ventricular defibrillation threshold. Dogs were anesthetized with pentobarbital and subjected to repeated fibrillation-defibrillation episodes. Defibrillation thresholds were determined at 15-min intervals using underdamped 5-6 msec sinusoidal current shocks, from 30 min before drug injection to 120 min after injection. Eight dogs were given clofilium phosphate (0.34 mg/kg, iv). Another 10 dogs were given bretylium tosylate (10.0 mg/kg, iv). Both drugs lowered defibrillation threshold from 15-90 min after injection. The maximum clofilium effect was a 31% decrease in threshold current and a 54% decrease in threshold energy. The greatest decrease in defibrillation threshold produced by bretylium was 16% for current and 31% for energy. These drug induced changes in defibrillation threshold are of potential clinical benefit, if they occur in human subjects at doses that are effective for control of ventricular arrhythmias.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The effect of newer antiarrhythmic drugs on defibrillation threshold

Tacker

Niebauer

Babbs

et al. 1980

Critical Care Medicine

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“…THE mechanisms of action of antiarrhythmic drugs were discussed in these reviews over a decade ago (Rosen and Hoffman, 1973). Since then, important new concepts of the blocking action of drugs have been proposed and tested experimentally.…”

mentioning

confidence: 99%

Antiarrhythmic drug action. Blockade of the inward sodium current.

Grant¹,

Starmer²,

Strauss³

1984

Circulation Research

151

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“…Class I antiarrhythmic drugs such as quinidine and disopyramide typically decrease excitability, reduce dV/dt of phase 0, and prolong action potential duration and refractory period (Rosen and Hoffman, 1973;Hauswirth and Singh, 1979). However, it has yet to be determined which, if any, of these electrophysiological parameters most importantly determines antiarrhythmic drug effect.…”

Section: Discussionmentioning

confidence: 99%

Electrophysiological effects of the optical isomers of disopyramide and quinidine in the dog. Dependence on stereochemistry.

Mirro¹,

Watanabe²,

Bailey³

1981

Circulation Research

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SUMMARY We studied the electrophysiological effects of the optical isomers of disopyramide and quinidine on canine cardiac Purkinje fibers. Conventional microelectrode techniques were employed to study the effects of racemic disopyramide, (+)-disopyramide, (-)-disopyramide, quinidine, and quinine. Racemic disopyramide, (+)-disopyramide, and quinidine prolonged action potential duration (APD) measured at 90% repolarization. In contrast, (-)-disopyramide and quinine shortened APD. These directionally opposite effects on repolarization were observed throughout 60 minutes exposure to drug and were concentration-dependent. All five compounds reduced dV/dt of phase 0, increased conduction time, and increased the current requirement for all-or-none depolarization. The effects of all five compounds on dV/dt, conduction time, and current requirements were time-and concentration-dependent. Our results indicate that the stereochemical configurations of disopyramide and quinidine determine their effects on repolarization of cardiac Purkinje fibers. Circ Res 48: 867-874, 1981

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Mechanisms of Action of Antiarrhythmic Drugs

Cited by 138 publications

References 9 publications

The effect of newer antiarrhythmic drugs on defibrillation threshold

The effect of newer antiarrhythmic drugs on defibrillation threshold

Antiarrhythmic drug action. Blockade of the inward sodium current.

Electrophysiological effects of the optical isomers of disopyramide and quinidine in the dog. Dependence on stereochemistry.

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