Prevention and Reversal of Ouabain‐induced Cardiotoxicity by Naloxone in the Guinea‐pig

Lee, A. Y. S.; Unang, T. W. K.; Wong, TM

doi:10.1111/j.1440-1681.1986.tb00315.x

Cited by 9 publications

(3 citation statements)

References 5 publications

(1 reference statement)

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“…Naloxone was found to accelerate the development of fatal cardiac arrhythmias (Rabkin & Roob, 1986) suggesting that endogenous opioids are involved in digitalis‐induced arrhythmias an effect interrelated to the autonomic, mainly parasympathetic, nervous system. In contrast to these results, Lee, Unang & Wong (1986) showed that after pretreatment with naloxone, the dose of ouabain required to induce ventricular arrhythmias and cardiac arrest were significantly increased, in a dose‐dependent manner, compared with the control, indicating a protective effect of naloxone against digitalis intoxication. Administration of naloxone at the onset of cardiac arrhythmias induced by a lethal dose of ouabain restored the cardiac rhythm and consequently saved life, indicating an antiarrhythmic effect of naloxone in digitalis‐intoxicated guinea‐pigs (Lee et al.…”

Section: Central Opioid Receptorscontrasting

confidence: 74%

Cardiotoxicity of digitalis glycosides: roles of autonomic pathways, autacoids and ion channels

Demiryürek

2005

Auton Autocoid Pharmacol

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1 Cardiac glycosides have been used for centuries as therapeutic agents for the treatment of heart diseases. In patients with heart failure, digoxin and the other glycosides exert their positive inotropic effect by inhibiting Na(+)-K(+)-ATPase, thereby increasing intracellular sodium, which, in turn, inhibits the Na(+)/Ca(2+) exchanger and increases intracellular calcium levels. As the therapeutic index of digitalis is narrow, arrhythmias are common problems in clinical practice. The mechanisms and mediators of these arrhythmias, however, are not completely understood. 2 The involvement of the sympathetic and parasympathetic nervous system in digitalis cardiac toxicity is reviewed. 3 Receptors, channels, exchange systems or other cellular components involved in digitalis-induced cardiotoxicity are also reviewed. 4 Possible mediators of digitalis-induced cardiac toxicity are discussed. 5 Management of digitalis toxicity in patients is summarized. 6 The determination of the possible mediators of digitalis-induced cardiac toxicity will enhance our knowledge and lead to the development of new therapeutic strategies to treat these lethal arrhythmias.

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Section: Central Opioid Receptorscontrasting

confidence: 74%

Cardiotoxicity of digitalis glycosides: roles of autonomic pathways, autacoids and ion channels

Demiryürek

2005

Auton Autocoid Pharmacol

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“…Similar antiarrhythmic activity of naloxone was later described in other species with various experimental models (Huang et al, 1986;Lee et al, 1986). The accepted explanation for this action of naloxone is the blockade of opioid receptors which prevents the putative disturbing effects of endogenous opioid peptides.…”

Section: Introductionmentioning

confidence: 57%

“…The opioid antagonist, naloxone, has been shown previously to reduce the incidence and severity of cardiac arrhythmias resulting from coronary ligation in rats (Fagbemi et al, 1982). Similar antiarrhythmic activity of naloxone was later described in other species with various experimental models (Huang et al, 1986;Lee et al, 1986). The accepted explanation for this action of naloxone is the blockade of opioid receptors which prevents the putative disturbing effects of endogenous opioid peptides.…”

Section: Introductionmentioning

confidence: 68%

Anti‐arrhythmic activities of opioid agonists and antagonists and their stereoisomers

Sarne¹,

Flitstein²,

Oppenheimer³

1991

British J Pharmacology

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1 A series of opioid agonists, antagonists and their (+)-stereoisomers were tested for antiarrhythmic activity in the rat coronary artery occlusion model. 2 Naloxone (0.01-2mgkg-') significantly reduced the incidence and severity of cardiac arrhythmias, in accordance with previous published studies. 3 The non-opioid stereoisomer, (+)-naloxone, was equipotent with naloxone against occlusion-induced arrhythmia. 4 Similar non-stereospecific antiarrhythmic effects were induced by another opioid antagonist, Win 44,441-3 and its stereoisomer Win 44,441-2. 5 The opioid agonists, morphine and levorphanol, protected against occlusion-induced arrhythmia as did the opioid antagonists, and the (+ )-stereoisomer, dextrorphan, was equipotent to levorphanol. 6 It is concluded that the antiarrhythmic effects of opioid drugs are not mediated by opioid receptors. A direct effect on ionic currents in cardiac muscle is suggested as the mechanism of opioid antiarrhythmic activity.

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Antiarrhythmic action of naloxone: Direct, non-opiate effect on the rat heart

et al. 1988

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Prevention and Reversal of Ouabain‐induced Cardiotoxicity by Naloxone in the Guinea‐pig

Cited by 9 publications

References 5 publications

Cardiotoxicity of digitalis glycosides: roles of autonomic pathways, autacoids and ion channels

Cardiotoxicity of digitalis glycosides: roles of autonomic pathways, autacoids and ion channels

Anti‐arrhythmic activities of opioid agonists and antagonists and their stereoisomers

Antiarrhythmic action of naloxone: Direct, non-opiate effect on the rat heart

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