Antiarrhythmic evaluation of naloxone against acute coronary occlusion-induced arrhythmias in pigs

Bergey, James L.; Beil, Michael E.

doi:10.1016/0014-2999(83)90566-6

Cited by 28 publications

(17 citation statements)

References 7 publications

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“…In the study on pigs by Bergey & Beil (1983), the body weights ranged from 7-14kg, which are of a similar order of magnitude to that of the dogs used in this study (5-10 kg). Therefore, the sizes ofheart in the two experimental animals used in these two studies are not greatly different.…”

mentioning

confidence: 74%

“…This antiarrhythmic effect of naloxone in the rat was supported by our study using an isolated heart preparation (Zhan et al, 1986) although this effect was found to be absent in anaesthetized pigs also subject to acute coronary ligation (Bergey & Beil, 1983). In order to determine whether the discrepancy in the action of naloxone on arrhythmias in the rat and pig is due to species difference or size ofthe heart, we have studied the effect of naloxone in anaesthetized dogs with arrhythmias induced by acute coronary ligation followed by reperfusion.…”

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confidence: 91%

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Naloxone inhibits arrhythmias induced by coronary artery occlusion and reperfusion in anaesthetized dogs

Huang¹,

Lee²,

Wong³

et al. 1986

British J Pharmacology

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The intravenous administration ofnaloxone 2 min before coronary artery occlusion in anaesthetized dogs reduced the incidence and severity of cardiac arrhythmias during coronary occlusion (20 min) and reperfusion (120 min) in a dose-related manner. It also reduced the mortality. At a dose of 1 mg kg-' (the maximum dose used in this study) naloxone abolished the appearance of the life threatening ventricular fibrillation (VF) and ventricular tachycardia (VT) and as a consequence all dogs in this group survived. The results suggest a possible involvement ofendogenous opioid peptides in arrhythmogenesis during coronary occlusion and reperfusion in the dog.Introduction It has been shown that naloxone inhibits the early arrhythmias resulting from acute coronary ligation in conscious and anaesthetized rats (Fagbemi et al., 1982). This antiarrhythmic effect of naloxone in the rat was supported by our study using an isolated heart preparation (Zhan et al., 1986) although this effect was found to be absent in anaesthetized pigs also subject to acute coronary ligation (Bergey & Beil, 1983). In order to determine whether the discrepancy in the action of naloxone on arrhythmias in the rat and pig is due to species difference or size ofthe heart, we have studied the effect of naloxone in anaesthetized dogs with arrhythmias induced by acute coronary ligation followed by reperfusion.

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confidence: 74%

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confidence: 91%

Naloxone inhibits arrhythmias induced by coronary artery occlusion and reperfusion in anaesthetized dogs

Huang¹,

Lee²,

Wong³

et al. 1986

British J Pharmacology

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“…In animal studies, however, the situation is different. Doses up to 10mg kg-' naloxone have been injected intravenously to increase blood pressure during experimental shock (Holaday, 1983) or to prevent arrhythmias (Fagbemi et al, 1982;Bergey & Beil, 1983). This is certainly sufficient to reach plasma concentrations around 5 fig ml-' for 15-30 min (Ngai et al, 1976;Pace et al, 1979).…”

Section: Discussionmentioning

confidence: 99%

“…In anaesthetized rats, naloxone enhanced noradrenaline-induced arrhythmias (Rabkin & Fung, 1984) but prevented disorders of rhythm resulting from coronary artery ligation (Fagbemi et al, 1982). In pigs, on the other hand, the drug was ineffective against occlusion-induced arrhythmias (Bergey & Beil, 1983). More than one explanation can be offered for the influence of naloxone on the cardiac rhythm.…”

Section: Introductionmentioning

confidence: 99%

Influence of the optical isomers (+)‐ and (−)−naloxone on beating frequency, contractile force and action potentials of guinea‐pig isolated cardiac preparations

Brasch

1986

British J Pharmacology

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1 Naloxone in concentrations ranging from 7.5 to 120 Amol I1 reduced the beating frequency of guinea-pig isolated atria. The ED50 was 7.9 gLmol 1-P' for the (-) 4 The influence ofmorphine (120 ;Lmol I') on papillary muscle AP was small. AP duration and FRP showed a marginal prolongation while V,,.l was slightly decreased. (-)-Naloxone 60 pmol I`had no effect on slow-response APs of K+-depolarized papillary muscles. Slow-response APs were abolished by verapamil (I pmol I').6 In left atrial strips the prolongation of the AP duration produced by 120 1tmol 1-of either (-)-or (+ )-naloxone resembled the drug effect in papillary muscles. 7 Most of the observed changes can be explained by an inhibition of the time-dependent membrane K+ outward current, an effect of naloxone that may be classified as a Class III antiarrhythmic action.Apparently this effect is not mediated by stereospecific opioid receptors.

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“…However, our data contradict the results of other investigators who found antiarrhythmic effects of opioid receptor antagonists during cardiac ischemia and reperfusion. [23][24][25][26] The opioid receptor antagonists exhibited antiarrhythmic properties both in vivo 23,24 and in vitro in experiments with isolated rat heart. 24,26 The first report on the antiarrhythmic properties of naloxone was published in 1983 by Bergey and Beil 23 who performed experiments with anesthetized pigs.…”

Section: Discussionmentioning

confidence: 99%

Activation of Peripheral Delta Opioid Receptors Increases Cardiac Tolerance to Arrhythmogenic Effect of Ischemia/Reperfusion

Maslov

Oeltgen

Lishmanov

et al. 2014

Academic Emergency Medicine

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Objectives: The objective of this study was to investigate the role of peripheral l, d 1 , d 2 , and nociceptin opioid receptors agonists in the regulation of cardiac tolerance to the arrhythmogenic effect of ischemia/ reperfusion in rats.Methods: Anesthetized open-chest male Wistar rats were subjected to either 45 minutes of left coronary artery occlusion (phase 1a 10 minutes and phase 2b 35 minutes) and 2 hours of reperfusion in Experiment 1 or 10 minutes of ischemia and 10 minutes of reperfusion in Experiment 2. In Experiment 1, saline or vehicle controls and the mu-specific opioids dermorphin-H (Derm-H) and ([D-Ala2, N-Me-Phe4, Gly-ol5] enkephalin (DAMAGO); the delta-1-specific opioid D-Pen2,5enkephalin (DPDPE); nociceptin; and the delta-2-specific opioids deltorphin-II (Delt-II), Delt-Dvariant (Delt-Dvar), and deltorphin-E (Delt-E) were infused 15 minutes prior to ischemia. In Experiment 2, DPDPE, Delt-D, Delt-Dvar, and Delt-E were infused at 15 minutes prior to ischemia. The universal opioid receptor antagonist naltrexone, the peripherally acting antagonist naloxone methiodide, the selective d 1 antagonist 7-benzylidene naltrexone maleate, and the specific d 2 antagonist naltriben mesylate were infused 25 minutes prior to ischemia.Results: In Experiment 1, pretreatment with the l opioids Derm-H and DAMGO, DPDPE, and nociceptin at all doses tested did not reduce the incidence of ischemia-induced arrhythmias compared to controls during 45 minutes of ischemia. The d 2 opioids Delt-II (0.12 mg/kg), Delt-Dvar (0.3 mg/kg), and Delt-E (0.18 mg/kg) all demonstrated significant antiarrhythmic effects at the 150 nmol/kg dose compared to saline or vehicle controls. Nine of 19 animals treated with Delt-II were tolerant without ventricular arrhythmias to the arrhythmogenic effect of ischemia during the first 10 minutes of ischemia (phase 1a) and 11 of 19 were without ventricular arrhythmias during the following 35 minutes of ischemia (phase 1b). Delt-II also decreased the incidence of premature ventricular contractions and ventricular tachycardia by almost half during phase 1a. Delt-II did not affect the incidence of ventricular fibrillation (VF). Pretreatment with DeltDvar and Delt-E completely blocked the incidence of VF in phase 1b. Delt-E also decreased premature ventricular contractions by 50%, and the incidence of ventricular tachycardia decreased over twofold in phase 1b of ischemia. There was no enhanced tolerance by any of the delta-2 opioids to the arrhythmogenic effect of reperfusion after long-term ischemia. In Experiment 2, after 10 minutes of ischemia and 10 minutes of reperfusion, Delt-II (0.12 mg/kg) reduced the incidence of premature ventricular contractions and ventricular tachycardia compared to controls, and completely blocked the incidence of VF following 10 minutes of reperfusion. Delt-Dvar and Delt-E were without effect, as was DPDPE following 10 minutes of reperfusion. The antiarrhythmic effect of Delt-II during 10 minutes of ischemia and 10 minutes of reperfusion was completely blocked ...

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Antiarrhythmic evaluation of naloxone against acute coronary occlusion-induced arrhythmias in pigs

Cited by 28 publications

References 7 publications

Naloxone inhibits arrhythmias induced by coronary artery occlusion and reperfusion in anaesthetized dogs

Naloxone inhibits arrhythmias induced by coronary artery occlusion and reperfusion in anaesthetized dogs

Influence of the optical isomers (+)‐ and (−)−naloxone on beating frequency, contractile force and action potentials of guinea‐pig isolated cardiac preparations

Activation of Peripheral Delta Opioid Receptors Increases Cardiac Tolerance to Arrhythmogenic Effect of Ischemia/Reperfusion

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