Electrophysiologic effects of blocking and stimulating the opioid system in patients with unexplained heart palpitations

Markiewicz, K; W, Kuś; M, Cholewa; Bubiński, R

doi:10.1002/clc.4960141008

Cited by 8 publications

(3 citation statements)

References 19 publications

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“…It has been reported to lengthen the sinoatrial, intra-atrial and atrioventricular node conduction times, and to prolong the atrial and atrioventricular node effective refractory periods. 22) In this study, naloxone produced an antiarrhythmic effect without affecting MAP or HR, suggesting that the blocking effect of naloxone against picrotoxin-induced arrhythmias is not secondary to changes in MAP or HR. It also suggests that antiarrhythmic doses of naloxone may not alter hemo- …”

Section: Figure 1 Andsupporting

confidence: 49%

Antiarrhythmic Action of Naloxone. Suppression of Picrotoxin-Induced Cardiac Arrhythmias in the Rat.

et al. 1992

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SUMMARYThe antiarrhythmic properties of the opiate antagonist naloxone have been reported in a variety of models of arrhythmia. To determine the generality and the possible central involvement of its antiarrhythmic activity, the effects of naloxone were assessed against cardiac arrhythmias induced by intravenous bolus injections of picrotoxin. Naloxone at doses of 0.33 and 1mg/kg significantly reduced the incidence and severity of picrotoxin-induced arrhythmias in a dose-related manner, without alteration of blood pressure and heart rate. The results demonstrate the antiarrhythmic efficacy of naloxone in an additional animal model. They further suggest that the antiarrhythmic actions of naloxone may be mediated by the central nervous system via both the autonomic and GABAergic pathways. 2). The pure opiate antagonist naloxone has also been shown to inhibit arrhythmias resulting from (1) coronary artery occlusion in rats3) and dogs,4) (2) ouabain in guinea pigs,5),6) (3) adrenaline7) or chloroform-hypoxia8) in rats and (4) ischemia-reperfusion in isolated rat hearts.9),10) These findings indicate that naloxone possesses antiarrhythmic properties.On the other hand, Bergey and Beil11) observed no antiarrhythmic action of naloxone in the anesthetized pig subjected to coronary arterial ligation. This study tested the antiarrhythmic activity of naloxone against picrotoxin-induced centrogenic arrhythmias in the rat.

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Section: Figure 1 Andsupporting

confidence: 49%

Antiarrhythmic Action of Naloxone. Suppression of Picrotoxin-Induced Cardiac Arrhythmias in the Rat.

et al. 1992

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“…In the only previous study of the cardiac electrophysiological effects of naloxone in human subjects, naloxone and pentazocine were administered in sequence, intravenously, in a single dose of 30 ,ug kg-' over 10 min to 20 patients undergoing electrophysiological study for the assessment of palpitations [18]. This dose is approximately 1000 times less than that which we employed.…”

Section: Resultsmentioning

confidence: 98%

Failure to reproduce the in vitro cardiac electrophysiological effects of naloxone in humans.

Oldroyd¹,

Rankin²,

Gray³

et al. 1994

Brit J Clinical Pharma

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1 Opioid receptor antagonists such as naloxone have shown antiarrhythmic activity in animal models of coronary artery occlusion. Studies have indicated that these effects are stereospecific but both isomers of naloxone prolong action potential duration and refractoriness in guinea-pig and rabbit isolated ventricular myocardium (Class III effect). 2 This study was performed to identify whether this Class III effect of naloxone could be reproduced in human myocardium in vivo. Twenty patients with coronary artery disease received intravenous racemic naloxone (1-40 ,ug kg-' min-'). Surface electrocardiographic parameters were measured and refractory periods were determined during fixed rate pacing by programmed stimulation. 3 The corrected QT interval during sinus rhythm (SR-QTc) was prolonged by 5(3)% (P = 0.06) at a dose of 20 ,ug kg-' min-' and by 9(10)% at 40 ,ug kg-' min-' (P = 0.03).These small changes were lost at higher paced heart rates. No significant effects on atrial, atrioventricular nodal or ventricular refractoriness were seen. 4 Plasma naloxone concentrations well into the micromolar range were achieved with both of the higher doses of naloxone administered. Plasma ,3-endorphin concentrations invariably increased following naloxone infusion. There was no statistical relationship between peak plasma naloxone concentrations and the absolute or percent prolongation of SR-QTc. 5 It seems unlikely that racemic naloxone would have any clinical utility as an antiarrhythmic agent. Racemic naloxone may enhance cardiac adrenergic nerve activity and this receptor mediated effect may have prevented the demonstration of any nonreceptor mediated prolongation of cardiac refractoriness. Studies with the individual stereoisomers of naloxone would be of interest.

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“…In addition, naloxone has a significant influence on the electrophysiological properties of the proximal part of the heart conduction system. It has been reported to lengthen the sinoatrial, intra-atrial and atrioventricular node conduction times, and to prolong the atrial and atrioventricular node effective refractory periods (Markiewicz et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

Stereospecific antiarrhythmic effects of naloxone against myocardial ischaemia and reperfusion in the dog

Lee

1992

British J Pharmacology

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1 The effects of both the (-)-and (+)-stereoisomers of naloxone in anaesthetized dogs with arrhythmias induced by acute coronary artery occlusion followed by reperfusion were investigated. 2 Following coronary artery occlusion and reperfusion, all dogs in the control group developed ischaemia-and reperfusion-induced cardiac arrhythmias, bradycardia and hypotension. 3 The opiate antagonist (-)-naloxone prevented the arrhythmias, bradycardia and hypotension due to myocardial ischaemia and reperfusion. 4 The (+)-stereoisomer of naloxone, which is inactive as an opiate antagonist, was without beneficial effects. 5 These results indicate a possible involvement of endogenous opioid peptides in the cardiac effects due to myocardial ischaemia and reperfusion, mediated by opiate receptors through opiate antagonism.

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Electrophysiologic effects of blocking and stimulating the opioid system in patients with unexplained heart palpitations

Cited by 8 publications

References 19 publications

Antiarrhythmic Action of Naloxone. Suppression of Picrotoxin-Induced Cardiac Arrhythmias in the Rat.

Antiarrhythmic Action of Naloxone. Suppression of Picrotoxin-Induced Cardiac Arrhythmias in the Rat.

Failure to reproduce the in vitro cardiac electrophysiological effects of naloxone in humans.

Stereospecific antiarrhythmic effects of naloxone against myocardial ischaemia and reperfusion in the dog

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