Antiarrhythmic effect ofRodiola rosea and its possible mechanism

Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 116, N ^o 8, pp. 175–176, August, 1993     

Cardioprotective effects of stimulation of peripheral μ-opiate receptors and the role of opiatergic mechanisms in the pathogenesis of stress-induced heart damage

Immobilization induces stress damage to the heart. DAGO, an agonist of μ-opiate receptors potentiates, while an agonist of peripheral μ-opiate receptors prevents this damage. Naltrexone reduces, while methylnaltrexone, an inhibitor of peripheral μ-opiate receptors, potentiates the stress-induced damage to the heart. Other opiate ligands have no effect on heart damage. It is suggested that the stress-induced damage to the heart is promoted by activation of central μ-opiate receptors and prevented by stimulation of peripheral μ-opiate receptors. Translated fromByulleten'Eksperimental'noi Biologii i Meditsiny, Vol. 123, No. 3, pp. 276–278, March, 1997     

Opiatergic mechanisms of the cardiotropic effect of acute cooling

Changes in myocardial contractility after an acute cold exposure following intracerebroventricular administration of opiate receptor agonists were studied in rat hearts isolated after Langendorff. Cold exposures were carried out individually for each animal in chambers at −10°C for 4 h. Thirty min before being exposed to cold the animals were administered in a brain ventricle 10 μl of μ- or δ-opiate receptor agonists (DAGO or DADLE, respectively). Isolation and perfusion of the hearts were performed directly after the cold exposure was over. The mechanism of reduction of myocardial contractility and coronary flow induced by an acute cold exposure is believed to include stimulation of μ-opiate receptors as one of its main components, and the effect of intracerebral hypertension on hemodynamic parameters is partially mediated through activation of δ-opiate receptors. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 118, N ^o 12, pp. 582–584, December, 1994 Presented by R. S. Karpov, Member of the Russian Academy of Medical Sciences     

Effect of ligands of opiate receptors on morphofunctional state of the sympathoadrenal system and electrical stability of the heart in acute cold exposure

Acute cold exposure (−20°C, 4 h) induces a transient decrease in the ventricular fibrillation threshold without morphological and radionuclide signs of irreversible damage to cardiomyocytes. The agonist of μ-receptors DAGO, which reduces adrenoreactivity of the myocardium, prevents the decrease in the ventricular fibrillation threshold induced by acute cold exposure. Translated fromByulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 123, No. 2, pp. 154–157, February, 1997     

Activation of k<Subscript>1</Subscript>-opioid receptor as a method for prevention of ischemic and reperfusion arrhythmias: Role of protein kinase C and K<Subscript>ATP</Subscript> channels

Intravenous pretreatment with κ-opioid receptor antagonist (−)-U-50,488 (1 mg/kg) improved heart resistance to the arrhythmogenic effect of coronary occlusion and reperfusion. Selective κ₁-opioid receptor antagonist norbinaltorphimine and nonselective blocker of peripheral opioid receptors methylnaloxone abolished this antiarrhythmic effect. Preliminary blockade of protein kinase C with chelerythrine or inhibition of ATP-dependent K⁺ channels (K_ATP channels) with glybenclamide abolished the antiarrhythmic effect of κ-opioid receptor activation. Selective inhibitor of sarcolemmal K_ATP channels did not modulate the κ-opioid receptor-mediated increase in cardiac electrical stability. Our results suggest that protein kinase C and mitochondrial K_ATP channels play an important role in the antiarrhythmic effect associated with activation of peripheral κ-opioid receptors. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 143, No. 2, pp. 145–148, February, 2007     

Takotsubo Syndrome: Clinical Manifestations,Etiology and Pathogenesis

The purpose of the review is the analysis of clinical and experimental data on the etiology and pathogenesis of takotsubo syndrome (TS). TS is characterized by contractile dysfunction, which usually affects the apical region of the heart without obstruction of coronary artery, moderate increase in myocardial necrosis markers, prolonged QTc interval (in 50% of patients), sometimes elevation of ST segment (in 19% of patients), increase N-Terminal Pro-B-Type Natriuretic Peptide level, microvascular dysfunction, sometimes spasm of the epicardial coronary arteries (in 10% of patients), myocardial edema, and life-threatening ventricular arrhythmias (in 11% of patients). Stress cardiomyopathy is a rare disease, it is observed in 0.6 - 2.5% of patients with acute coronary syndrome. The occurrence of takotsubo syndrome is 9 times higher in women, who are aged 60-70 years old, than in men. The hospital mortality among patients with TS corresponds to 3.5% - 12%. Physical or emotional stress do not precede disease in all patients with TS. Most of patients with TS have neurological or mental illnesses. The level of catecholamines is increased in patients with TS, therefore, the occurrence of TS is associated with excessive activation of the adrenergic system. The negative inotropic effect of catecholamines is associated with the activation of β₂ adrenergic receptors. An important role of the adrenergic system in the pathogenesis of TS is confirmed by studies which were performed using ¹²⁵I-metaiodobenzylguanidine (¹²⁵I -MIBG). TS causes edema and inflammation of the myocardium. The inflammatory response in TS is systemic. TS causes impaired coronary microcirculation and reduces coronary reserve. There is a reason to believe that an increase in blood viscosity may play an important role in the pathogenesis of microcirculatory dysfunction in patients with TS. Epicardial coronary artery spasm is not obligatory for the occurrence of TS. Cortisol, endothelin-1 and microRNAs are challengers for the role of TS triggers. A decrease in estrogen levels is a factor contributing to the onset of TS. The central nervous system appears to play an important role in the pathogenesis of TS.     

Possible mechanism underlying the antiarrhythmic effect of peptides nociceptin and DALDA on the heart

During aconitine-induced arrhythmias the antiarrhythmic effect of DALDA (Tyr-D-Arg-Phe-Lys-NH2) and nociceptin (orphanin FQ) administered intravenously depended on activation of nitric oxide synthase. KATP channels were not involved in the realization of this effect. Endogenous prostanoids played a minor role in the antiarrhythmic effect of nociceptin and did not contribute to the protective influence of DALDA. The antiarrhythmic effect of orphanin FQ administered intravenously did not depend on functional activity of the autonomic nervous system. However, the effect of orphanin FQ after intracerebroventricular infusion was determined by changes in the state of this system.