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

Sarne, Yosef; Flitstein, A.; Oppenheimer, Edna

doi:10.1111/j.1476-5381.1991.tb12235.x

Cited by 30 publications

(14 citation statements)

References 10 publications

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“…Indeed, Sarne et al (1991) demonstrated antiarrhythmic effect of both L-naloxone, which inhibits ORs, and its D-isomer, which cannot bind to them. In contrast, we used the lowest applicable doses of OR antagonists, which minimized their nonspecific effect.…”

Section: Discussionmentioning

confidence: 97%

Contribution of the Endogenous Opioid System to Regulation of Heart Resistance to the Arrhythmogenic Effect of Short-term Ischemia and Reperfusion

Maslov

Liishmanov

Budankova

et al. 2005

Biol Bull Russ Acad Sci

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Preliminary selective blockade of µ , δ 1 , δ 2 , κ 1 , and κ 2 opioid receptors proved to have no effect on the incidence of ventricular arrhythmias during a 10-min coronary occlusion and subsequent reperfusion in ketamine-anesthetized rats. We propose that the endogenous opioid system has no considerable role in regulation of heart resistance to the arrhythmogenic effect of short-term local ischemia and subsequent reperfusion.

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Section: Discussionmentioning

confidence: 97%

Contribution of the Endogenous Opioid System to Regulation of Heart Resistance to the Arrhythmogenic Effect of Short-term Ischemia and Reperfusion

Maslov

Liishmanov

Budankova

et al. 2005

Biol Bull Russ Acad Sci

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show abstract

“…Further, the incidence and severity of ischaemia and reperfusion-induced arrhythmias are reduced by the opioid receptor antagonists naloxone (Sarne et al, 1991) and MR 2266 (Wong et al, 1990). Other studies suggest that K-receptor blockade may be antiarrhythmic whereas buprenorphine, an agent with mixed actions on p-and K-receptors, may exert antiarrhythmic effects directly, independent of opioid receptors (Boachie-Ansah et al, 1989).…”

Section: Introductionmentioning

confidence: 90%

Cardiovascular actions of the κ‐agonist, U‐50,488H, in the absence and presence of opioid receptor blockade

Pugsley

Penz

Walker

et al. 1992

British J Pharmacology

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1 The cardiovascular actions of U-50,488H, a K-receptor agonist, were studied in rat isolated perfused hearts, and in anaesthetized rats, over concentrations or doses generally above those required to produce K-receptor-mediated effects. 2 U-50,488H dose-dependently decreased left-ventricular peak systolic pressure and beating rate in vitro and reduced blood pressure and heart rate in vivo. 3 Over the concentration range of 1-30UM in vitro, and the dose-range of 0.5-32,umolkg-1 in vivo, U-50,488H prolonged the P-R, QRS and Q-T intervals of the ECG. 4 The effects of U-50,488H were not antagonized by an opioid receptor antagonist, naloxone (1 pM or 8/,amolkg-1). Similarly, the opioid receptor antagonist, MR 2266, at 8 pmolkg-1 did not significantly reduce the cardiovascular actions of U-50,488H in vivo. 5 The actions of U-50,488H on responses to electrical stimulation were also studied. Over the dose range of 0.5-32,amol kg-1, U-50,488H altered thresholds and effective refractory period. It had a biphasic action on thresholds for induction of ventricular fibrillation. Thresholds were decreased at lower doses (0.5-4pmol kg 1) but increased at higher doses (8-32 pmol kg l). The effects of lower doses were blocked by naloxone. Effective refractory period and threshold pulse width only increased with dose. 6 In conclusion, U-50,488H at high concentration, had direct depressant actions on cardiac contractility, electrical excitability and the ECG. These depressant effects were not antagonized by the opioid receptor antagonists, naloxone and MR 2266, and probably do not involve opioid receptors. Furthermore, some of the observed effects were those expected to result from sodium channel blockade.

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“…Arrhythmia was defined as ''more than 10 VPB or dysrhythmia incidence (VT or VF) of more than 10 seconds duration'' (Sarne et al, 1991).…”

Section: Electrocardiographic Analysesmentioning

confidence: 99%

The role of C-reactive protein in ischemia/reperfusion injury and preconditioning in a rat model of myocardial infarction

Valtchanova-Matchouganska¹,

Gondwe²,

Nadar³

2004

Life Sciences

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

Cited by 30 publications

References 10 publications

Contribution of the Endogenous Opioid System to Regulation of Heart Resistance to the Arrhythmogenic Effect of Short-term Ischemia and Reperfusion

Contribution of the Endogenous Opioid System to Regulation of Heart Resistance to the Arrhythmogenic Effect of Short-term Ischemia and Reperfusion

Cardiovascular actions of the κ‐agonist, U‐50,488H, in the absence and presence of opioid receptor blockade

The role of C-reactive protein in ischemia/reperfusion injury and preconditioning in a rat model of myocardial infarction

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