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Biomedical subjects

L N Maslov

Publications and source records attributed to L N Maslov.

At least 109 records · Page 6Linked to original sources
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[Interrelations between sympathetic adrenal and opioid systems--regulatory mechanism determining cardiac resistance to stress damage].

The present paper has analyzed relationship between sympatico-adrenal and opioid systems in the pathogenesis of stress heart damage. Based on the our own results and other investigator data the authors make a conclusion that namely relationship between opioid and sympatico-adrenal systems both on the level of the brain and on the periphery determines a degree of the heart resistance to the injury action of severe stress. Myocardial protection by opioids at stress was found to be mediated by the peripheral mu-opioid receptors and was associated with decrease in an activity of sympatico-adrenal system and a inhibition of its effector part. On contrary central opioid system activation leads to an increase in stress heart damage via an increase in sympathetical influence on the myocardium.

Adrenal Glands↗
PubMedDate not supplied

[Stimulation of peripheral delta1-opioid receptors as a method of preventing ischemic and reperfusion arrhythmia: role of K(ATP)-channels].

Preliminary administration of the delta 1-opioid receptor (delta 1-OR) peptide agonist DPDPE (0.5 mg/kg, i.v.) decreased the incidence of occlusion (10 min) and reperfusion (10 min) arrhythmias in rats. The delta 2-OR agonist DSLET did not affect arrhythmias upon the coronary artery occlusion and reperfusion. Pretreatment with the selective delta-antagonists ICI 174,864 (2.5 mg/kg) or TIPP[psi] (0.5 mg/kg) completely eliminated the antiarrhythmic effect of DPDPE. Uncapable of crossing the blood brain barrier, the nonselective OR antagonist naloxone methiodide (5 mg/kg) also abolished this effect. At the same time, hexametonium (10 mg/kg) did not antagonize the antiarrhythmic effect of DPDPE. Pretreatment with the KATP channel blocker glibenclamide (0.3 mg/kg) completely eliminated the protective effect of the delta 1-OR stimulation. It was concluded that the delta 1-OR stimulation prevents the ischemic and reperfusion arrhythmias by means of the KATP channel activation.

Animals↗
PubMedDate not supplied

[Stimulation of delta1-opioid receptors increases the ventricular fibrillation threshold in post-infarct cardiosclerosis: the role of K(ATP)-channels].

Preliminary administration of the delta 1-opioid receptor (delta 1-OR) selective peptide agonist DPDPE (0.1 mg/kg, i.v.) increased the ventricular fibrillation threshold (VFT) in postinfarction cardiosclerosis in rats. Pretreatment with the selective delta 1-OR antagonists ICI 174,864 (not affecting VFT) in a dose of 0.5 mg/kg completely eliminated the DPDPE-induced increase in the VFT. Pretreatment with the KATP channel selective blocker glibenclamide (0.3 mg/kg, i.v.) completely eliminated the delta 1-OR mediated increase in the VFT protective effect of the delta 1-OR stimulation. The intravenous injection of the mitochondrial KATP channel blocker 5-hydroxydecanoate (5 mg/kg) simultaneously with DPDPE not only eliminated the delta 1-OR mediated increase on VFT, but additionally increased the VBFT drop caused by cardiosclerosis. Injected separately, neither glibenclamide nor hydroxydecanoate affected the VFT level. It is concluded that stimulation of the delta 1-OR increases VFT by activating mitochondrial KATP-channels.

Adenosine Triphosphate↗
PubMedDate not supplied

[Anandamide and R-(+)-methanandamide prevent development of ischemic and reperfusion arrhythmia in rats by stimulation of CB2-receptors].

It has been found that prior intravenous administration of the endocannabinoid anandamide (10 mg/kg) or its synthetic analogue R-(+)-methanadamide (5 mg/kg) prevents a development of ischemic and reperfusion arrhythmias in rats. The prior injection of the CB1 receptor antagonist, SR 141716A (3 mg/kg), did no affect the antiarrhythmic action of both cannabinoids. Pretreatment with the CB2 receptor antagonist, SR 144528 (1 mg/kg), completely abolished antiarrhythmic effect of anandamide and R-(+)-methanandamide. Both CB antagonist had no effect on the arrhythmias itself. Pretreatment with the NO-synthase inhibitor, L-NAME (50 mg/kg), had no effect on the antiarrhythmic action of cannabinoids. We therefore conclude that CB2 receptor stimulation increases the heart tolerance to ischemic and reperfusion arrhythmias.

Animals↗
PubMedDate not supplied

[The opiatergic link between the antiarrhythmic effect of adaptation and hypoxia in the model of ischemia and reperfusion in vivo].

Rat adaptation to repeated periods of hypobaric hypoxia has been found to prevent the occurrence of ischemic and reperfusion ventricular arrhythmias on a 10-minte coronary artery occlusion model. Inhibition of delta-opioid receptors by intravenous administration of the selective delta-opioid antagonist TIPP (psi) in a dose of 0.5 mg/kg, intravenously (i.v.), completely abolished the antiarrhythmic effect of adaptation to hypoxia. Inhibition of mu-opioid receptors by CTAP (0.5 mg/kg, i.v.) or kappa-receptors by nor-binaltorphimine (9 mg/kg i.v.) had no effect on the incidence cardiac rhythm disturbances in adapted rats during coronary artery occlusion and reperfusion. Therefore, these findings suggest that delta-opioid receptors play an important role in inhibiting arrhythmia formation in this model.

Adaptation, Physiological↗
PubMedDate not supplied

[The mechanism of the antiarrhythmic action of dalargin in experimental myocardial ischemia].

It has been found that injection of dalargin before the occlusion of the left anterior coronary artery prevents an increase of cAMP content in the myocardium and blood plasma. In the myocardium of rats given dalargin before acute myocardial ischemia, the content of cGMP was increased and the level of somatostatin was reduced. It is assumed that the increase of the content of cGMP and the reduction of cAMP and somatostatin levels in the myocardium play an important role in antiarrhythmic action of dalargin.

Animals↗
PubMedDate not supplied

[Role of the opioid system in prevention of ischemic disorders of cardiac rhythm during adaptation to cold and physical exertion in rats].

It was found that adaptation of rats to cold and physical exercise prevented ventricular fibrillation caused by occlusion of the left anterior coronary artery. Adaptation to cold or only to physical exercise did not prevent ventricular arrhythmias. A significant increase of the beta-endorphin content in the hypophysis and hypothalamus was demonstrated in all adapted rats. An increased content of meth-enkephalin (ME) in the myocardium was found only in rats adapted to cold and physical exercise. It is suggested that increase of the myocardial ME content is of essential significance in the antiarrhythmic action of adaptation.

Adaptation, Physiological↗
PubMedDate not supplied

[Change in the opioid peptide level in the heart and blood plasma during acute myocardia ischemia complicated by ventricular fibrillation].

After occlusion of the anterior descending coronary artery content of opioid peptides was increased 2-3-fold in blood plasma of all the rats with and without ventricular fibrillation. Content of Leu-enkephalin was decreased in ischemic and non-ischemic regions of myocardium under conditions of ventricular fibrillation. At the same time, concentration of Met-enkephalin in myocardium was increased in the acute ischemia independently on the effect of fibrillation. Synthetic enzyme-resistant derivative of Leu-enkephalin, administered before acute myocardial ischemia, prevented a decrease in the ventricular fibrillation threshold caused by the occlusion. Alteration of the Leu-enkephalin content in heart tissue appears to be importance in pathogenesis of ventricular fibrillation developed after acute myocardial ischemia.

Acute Disease↗
PubMedDate not supplied

[Central effects of ORL1 receptor ligands].

It has been discussed literature data on molecular structure of ORL1 receptor and its interaction with intracellular signal systems and neurotransmitters. Data on chemical structure of ORL1 receptor ligands and their central effects (nociception, locomotion, feeding, cognition) are presented.

Animals↗
PubMedDate not supplied

[Peripheral effects of ligands of ORL1 receptors].

It has been discussed literature data on the role for ORL1 (NOR) receptors in the regulation of function of gastrointestinal, respiratory, cardiovascular, immune, endocrine systems. In addition, it has been discussed a possibility of penetration of blood brain barrier for ORL1 receptor ligands and species dependence of NOR-ligands' effects.

Animals↗
PubMedDate not supplied

[The role of opiate receptors and ATP-dependent potassium channels of mitochondria in the formation of myocardial adaptive resistance to the arrhythmogenic effect of ischemia and reperfusion].

Preliminary stimulation of opiate receptors (ORs) by intravenous administration of mu agonist DALDA (0.5 mg/kg), delta 1 agonist DPDPE (0.5 mg/kg), and kappa agonist (-)-U-50.488 (1 mg/kg) increases rat myocardial resistance to arrhythmogenic effect of coronary occlusion (10 min) and reperfusion (10 min). Activation of delta 2 ORs (DSLET, 0.5 mg/kg) has no effect on the incidence rate of ischemic and reperfusion arrhythmias. Preliminary administration of glibenclamide (0.3 mg/kg), an inhibitor of KATP channels, blocks the antiarrhythmic effect of DALDA and DPDPE. Repeated short-term exposures of rats to immobilization within two weeks increases the heart tolerance to the arrhythmogenic effect of coronary occlusion and reperfusion. This effect disappears after administration of CTAP (0.5 mg/kg), a mu antagonist, or injection of 5-hydroxydecanoate (5 mg/kg), an inhibitor of mitochondrial KATP channels. The selective antagonists of delta and kappa ORs have no effect on cardiac adaptation-induced resistance to the arrhythmogenic effect of ischemia and reperfusion. We believe that stimulation of mu, delta, and kappa ORs increases myocardial tolerance to the arrhythmogenic effect of ischemia and reperfusion through activation of KATP channels. The antiarrhythmic effect of the adaptation is mediated by stimulation of mu ORs and mitochondrial KATP channels.

Adaptation, Physiological↗
PubMedDate not supplied

[The role of delta-1 opiate receptors in regulation of contractility in isolated rat heart during normal oxygenation and ischemia-reperfusion].

The experiments on isolated rat heart demonstrated significant decrease in reperfusion-induced damage of cardiomyocytes by addition of selective delta 1 receptor agonist DPDPE (0.1 mg/l) to the perfusion solution. On the contrary, no cardioprotective effect was observed for 0.5 mg/l concentration of the peptide or after its intravenous injection. Stimulation of the cardiac delta 1 opioid receptors by intravenous injection of 0.5 mg/kg DPDPE or its addition to the perfusion solution decreased myocardial contractility both in conditions of normal oxygenation and during reperfusion. Thus, the cardioprotective and negative inotropic effect of DPDPE is mediated by activation of the cardiac delta 1 opioid receptors.

Animals↗
PubMedDate not supplied

[Stimulation of the delta 1-receptors help to decrease reperfusion induced myocardial stunning].

In vivo or in vitro administration of a omega 1 receptor agonist d-SKF 10,047 (1 mg/kg intravenously or 10 mg/l in vitro) promoted an increase in the resistance of isolated perfused rat heart to ischemia/reperfusion injury. Both in vivo and in vitro stimulation of omega receptors prevents development of reperfusion contracture and release of creatine kinase and increases the developed pressure, double product, +dP/dt, and -dP/dt in the left ventricle. Activation of omega receptors has no significant effect on the occurrence of reperfusion arrhythmias ex vivo. Stimulation of cardiac sigma receptors is proposed to prevent myocardial stunning.

Animals↗
PubMedDate not supplied

[The effect of K(ATP)-channel activation on the electrical stability of myocardium in rats with postinfarction cardiosclerosis].

Opening of the ATP-dependent K-channels (K(ATP) channels) upon intravenous administration of the cardioselective activator BMS 180448 (3 mg/kg) decreased the ventricular fibrillation threshold (VFT) in rats with postinfarction cardiosclerosis (PIC). Preliminary injection of the selective K(ATP) channel blocker glibenclamide (0.3 mg/kg, i.v.) completely abolished the profibrillatory effect of BMS 180448. At the same time, the mitochondrial K(ATP) channel blocker 5-hydroxydecanoic acid (5 mg/kg) did not influence the proarrhythmogen activity of BMS 180448. Simultaneous administration of the sarcoK(ATP) channel inhibitor HMR 1098 (3 mg/kg) and BMS 180448 increased the VFT up to a level in intact animals. Administration of the mitoK(ATP) channel activator diazoxide (5 mg/kg) after preliminary treatment with guanethidine (50 mg/kg) increased the VFT in rats with PIC. It is concluded that opening of the mitoK(ATP) channels increases the cardiac electrical stability in rats with PIC.

Adenosine Triphosphate↗