Quinidine toxicity and its treatment

Luchi, Robert J.; Helwig, John; Conn, Hadley L.

doi:10.1016/0002-8703(63)90008-5

Cited by 46 publications

(12 citation statements)

References 11 publications

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“…Quinidine has some beta-receptor-blocking activity (14), although this may not be the only way its cardiodepressant effects are mediated. One possible conclusion to be drawn from our results is that beta-receptor blockade or depression of the force-velocity curve is related to impaired calcium uptake by sarcoplasmic reticulum but that antiarrhythmic activity relates to effects on membrane polarization-the one feature common to lidocaine, tetracaine, quinidine, and propranolol.…”

Section: Discussionmentioning

confidence: 99%

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A Qualitative Distinction between the Beta-Receptor-Blocking and Local Anesthetic Actions of Antiarrhythmic Agents

Shinebourne

White

Hamer

1969

Circulation Research

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Fragmented cardiac sarcoplasmic reticulum was isolated by differential centrifugation from canine myocardium. The effects of propranolol, quinidine, lidocaine (lignocaine) and tetracaine (amethocaine) on calcium uptake in sarcoplasmic reticulum in vitro were then measured. All the drugs are antiarrhythmic agents with local anesthetic activity, but propranolol and quinidine are known also to have beta-receptor-blocking actions in that they can prevent the cardiac effects of isoprenaline and depress the myocardium. Lidocaine and tetracaine do not generally depress the heart and had no effect on the calcium uptake, but propranolol and quinidine both significantly inhibited it. It was concluded that the antiarrhythmic actions of propranolol (and quinidine) may be independent of beta-receptor-blocking activity, and that the safety of lidocaine as an antiarrhythmic agent may be related to a lack of effect on the sarcoplasmic reticulum. ADDITIONAL KEY WORDSexcitation-contraction coupling calcium uptake sarcoplasmic reticulum myocardial contractility lidocaine propranolol tetracaine beta-receptor activity dog• The ability of propranolol and other sympathetic blocking drugs to decrease calcium uptake by cardiac sarcoplasmic reticulum and hence to interfere with excitationcontraction coupling has been suggested as an important cellular mechanism underlying sympathetic blockade (1-3). This and other work (4, 5) indicated that many drugs with a negative inotropic effect inhibit sarcotubular calcium uptake. As well as depressing myocardial contractility, propranolol, the most potent betareceptor-blocking agent, has local anesthetic and antiarrhythmic actions, and the question arose whether the antiarrhythmic effects were dependent on beta-receptor blockade or on some other nonspecific effect. It has been shown from measurements of intracellular potentials (6-8) that beta-receptor blockade and antiarrhythmic activity were not necessarily linked. It was concluded that changes From the Department of Cardiology, St. Bartholomew's Hospital, London, E. C. 1, England.Received January 23, 1969. Accepted for publication April 8, 1969. produced in transmembrane potentials thought to be related to arrhythmia suppression, such as a decrease in maximum rate of depolarization and a smaller overshoot, were independent of any action on beta-receptors.Lidocaine (lignocaine) is an effective antiarrhythmic agent but, unlike propranolol, is generally devoid of cardiodepressant activity (9-13), as is tetracaine (amethocaine), another potent local anesthetic. Quinidine, widely used to suppress arrhythmias, has local anesthetic and beta-receptor-blocking activity (14) and may depress the myocardium.We have attempted to clarify the relationship between antiarrhythmic activity and beta-receptor blockade by measurements of the effects of these agents on the calcium uptake of the isolated sarcoplasmic reticulum. MethodsSarcoplasmic reticulum was extracted by differential centrifugation from dog myocardium using a method previously described...

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Section: Discussionmentioning

confidence: 99%

“…Quinidine, widely used to suppress arrhythmias, has local anesthetic and beta-receptor-blocking activity (14) and may depress the myocardium.…”

mentioning

confidence: 99%

A Qualitative Distinction between the Beta-Receptor-Blocking and Local Anesthetic Actions of Antiarrhythmic Agents

Shinebourne

White

Hamer

1969

Circulation Research

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“…Most of the patients had rheumatic heart disease. Two studies compared carefully matched but separate groups of patients in sinus rhythm and atrial fibrillation and found that cardiac output averaged 18 and 20% higher in sinus rhythm (16,17).…”

Section: Discussionmentioning

confidence: 99%

“…Unless such variables as the time lapse between studies, metabolic state, heart rate, and concomitant drug therapy are kept constant, it is difficult to be sure that any change or lack of change after reversion is a reflection of rhythm alone. Adequate control of drug administration is especially important when quinidine is utilized, since the drug has myocardial depressant and peripheral vasodilator actions (18,19). The former might mask improvement after reversion, and the latter The present study was designed to control as many variables as possible.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic effects after reversion from atrial fibrillation to sinus rhythm by precordial shock.

Killip¹,

Baer²

1966

J. Clin. Invest.

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“…Molar sodium lactate (Bellet, 1963), sympathomimetics (Rokseth and Storstein, 1963;Linenthal and Zoll, 1963), calcium sodium versenate (Luchi et al, 1963), and external massage and direct-current shock (Rainier-Pope et al, 1962) are among the remedies that have been used either clinically or experimentally. In our patient the E.C.G.…”

Section: Commentmentioning

confidence: 99%