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Biomedical subjects

L N Maslov

Publications and source records attributed to L N Maslov.

At least 127 records · Page 7Linked to original sources
PubMedDate not supplied

[Antiarrhythmic and cardioprotective effect of stimulation of delta1-opiate receptors in myocardial ischemia and reperfusion].

Pretreatment with intravenous peptide delta1-opioid receptor (OR) agonist DPDPE (0.5 mg/kg) decreases the incidence of occlusion (10 min) and reperfusion (10 min) arrhythmias in rats. The agonist of delta2-OR DSLET has no effect on arrhythmias in coronary artery occlusion and reperfusion. Pretreatment with selective delta-antagonists ICI 174,864 (2.5 mg/kg) eliminates an antiarrhythmic effect of DPDPE. The addition of DPDPE to the perfusion solution in a final concentration of 0.1 mg/l and/or 0.5 mg/l fifteen min before ischemia also decreases the incidence of reperfusion arrhythmias in a concentration-dependent manner. The addition of DPDPE to the perfusion solution in a final concentration of 0.1 mg/l decreases creatine kinase levels in the coronary sinus effluent. However, DPDPE has no cardioprotective effect in a concentration of 0.5 mg/l or after intravenous administration. It is suggested that antiarrhythmic and cardioprotective effects of DPDPE during reperfusion may be due to stimulation of cardiac delta1-receptors.

Animals↗
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[Regeneration of myocardium].

It has been systematized modern data on the myocardial regeneration and the regulation of cardiac cell proliferation in mammals and man. It has been performed an analysis published works which indicate that cardiomyocyte division and DNA synthesis in myocardial cells increase in many times during different pathological conditions. It has been generalized and analyzed results of experimental and clinical researches on the participation of stem cells in the regeneration of the heart. It has been present literature data on the telomeres and telomerase in cardiomyocytes.

Animals↗
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[The effect of dalargin and des-Tyr-dalargin on the functional state of intact and ischemized-reperfused myocardium].

Experiments on isolated perfused rat heart showed that dalargin, an antagonist of mu- and delta-opioid receptors, favors a decrease in the parameters of contractility of intact myocardium, while not influencing the pumping function (systolic and diastolic contractility) of reperfused myocardium. At the same time, des-Tyr-dalargin (the non-opioid analog of dalargin) suppresses the contractility of both the intact heart and the isolated myocardium subjected to global ischemia and reperfusion. Both dalargin and des-Tyr-dalargin reduced the incidence of reperfusion-induced arrhythmia, but did not affect the coronary flow before ischemia and after restoration of the coronary flow. It is suggested that the effect of dalargin is related to activation of the cardiac delta-opioid receptors, while the inotropic action of des-Tyr-dalargin involves other receptor mechanisms.

Animals↗
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[Endogenic opioid peptides and antiarrhythmic effect of adaptation to stress].

Adaptation of rats to repeated short-term immobilization increases cardiac resistance to an arrhythmogenic action of coronary artery occlusion (10 min) and reperfusion (10 min) in rats anesthetized with ketamine and artificially ventilated. We examined the role of opioid receptors and endogenous opioid peptides in the development of this antiarrhythmic effect produced in response to repeated periods of immobilization stress. We found that repeated daily stress during a 15-day period resulted in an increase of leu-enkephalin in blood plasma, in the suprarenal gland and myocardium. Adaptation to stress also resulted in an increase in beta-endorphinl-31 in blood plasma, the hypophysis, hypothalamus and midbrain. Pretreatment with selective mu, delta and cappa opioid receptor (OR) antagonists had no effect on the incidence of occlusion and reperfusion-induced arrhythmias in non-adapted control rats. However, pretreatment with the selective muOR antagonist CTAP (0.5 mg/kg) intravenously completely abrogated the antiarrhythmic effect of adaptation. Selective delta and cappa receptor antagonists did not affect the antiarrhythmic effect of adaptation. Prior administration of the selective muOR agonist DALDA (0.1 mg/kg) decreased the incidence of occlusion and reperfusion-evoked arrhythmias in non-adapted rats. This effect was abolished by pretreatment with the selective muOR antagonist CTAP (0.5 mg/kg). These data suggest that mu opioid receptors and endogenous opioid peptides play an important role in the antiarrhythmic effect of adaptation to stress in rats.

Adaptation, Psychological↗
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[Delta-opioid receptor agonists prevent the irreversible damage of cardiomyocytes in ischemized-reperfused isolated rat heart].

Pretreatment with selective delta-opioid receptor (delta-OR) agonists decreased the level of creatine kinase in the coronary effluent of isolated rat heart during a 45-min global ischemia and a 30-min reperfusion. The effect was completely abolished after pretreatment of the delta-OR antagonist nitrindole. At the same time, pretreatment with mu-OR antagonists did not affect the level of creatine kinase in the coronary effluent. It is suggested that stimulation of the cardiac delta-OR prevents the irreversible cardiac cell damage during global ischemia and reperfusion in vitro. In contrast, the cardiac mu-OR do not play any significant role in regulation of the cardiac resistance to the pathogenic action of ischemia and reperfusion.

Analgesics↗
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[The mechanism of antiarrhythmic action of the endogenous ORL1 receptor agonist nociceptin].

Prophylactic intravenous (i.v.) injections of a selective agonist of ORL1 receptors nociceptin (orphanin FQ) in a dose of 0.4 mg/kg prevented the development of aconitine-induced arrhythmia in rats narcotized with diethyl ether or chloralose. Pretreatment with L-NAME (50 mg/kg) completely abolished this effect of orphanin FQ, while the pretreatment with indomethacin (10 mg/kg) only attenuated the agonist effect, rather than abolished it completely. At the same time, pretreatment with hexamethonium (10 mg/kg) or glibenclamide (3 mg/kg) had no effect on the nociceptin-dependent cardiac tolerance to the arrhythmogenic action of aconitine. Intracerebroventricular (i.c.v.) infusion of orphanin FQ (36 microg) also prevented the onset of aconitine-induced arrhythmia, but this effect was completely abolished by hexamethonium. It is concluded that the antiarrhythmic action of nociceptin with respect to aconitine-induced arrhythmia upon i.v. and i.c.v. administration is explained by different mechanisms. In the former case, the effect of orphanin FQ is related to the activation of NO synthase and cyclooxygenase, while the central action involves the vegetative nervous system.

Animals↗
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[The antiarrhythmic effect of (-)-U-50,488 in rats with acute ischemia and reperfusion of heart is mediated by kappa1-opioid receptor activation].

Pretreatment with a selective kappa1 opioid receptor (OR) agonist (-)-U-50,488 (1 mg/kg, i.v.) prevented the development of arrhythmias induced by occlusion (10 min) and reperfusion (10 min) in ketamine anesthetized rats, while the treatment with a less active enantiomer (+)-U-50,488 in the same dose produced no such effects. Preliminary intravenous administration of a selective kappa1 OR antagonist norbinaltorphimine (9 mg/kg) fully abolished the antiarrhythmic effect of (-)-U-50,488, while the kappa2 OR antagonist quadazocine (3 mg/kg) did not eliminate this effect. The injections of norbinaltorphimine or quadazocine alone did not influence the incidence of model arrhythmias caused by the occlusion and reperfusion. It was concluded that kappa1 OR stimulation favors an increase in cardiac tolerance to the arrhythmogenic action of occlusion and reperfusion.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMedDate not supplied

[Regulation by opiod peptides of the antioxidant enzyme activity and the prostanoid system in myocardium during stress].

The six hour stress in rats was modeled by the method of O. Desiderato. Cardiac damage was estimated by myocardial uptace of radioactive 99Tc-pyrophosphate. Intravenous administration of mixed mu and delta opioid receptor agonist, D- Ala2, Leu5, Arg6-enkephalin (dalargin), (non-penetrating through the blood brain barrier) at a dose of 0.1 mg/kg before stress decreased stress-induced 99Tc-pyroposphate uptake. Pretreatment with dalargin completely abolished the stress-induced increase in conjugated dienes and malondialdehyde levels in myocardium and prevented a decrease in total lipid soluble antioxidant levels in the heart after stress exposure. Stress is accompanied by an increase in activity of catalase, glutathione peroxidase, glutathione reductase and a decrease in activity of superoxide dismutase (SOD). Pretreatment with dalargin completely reversed stress-induced decrease in SOD activity but had minor effect on the activity of other antioxidant enzymes. Stress also resulted in an increase in myocardial content of thromboxane and a decrease in prostacycline and prostaglandin E levels in the heart. Pretreatment with dalargin completely eliminated these stress-induced changes in myocardial prostanoid levels. We propose that stress-induced heart injury depends on the activation of lipid peroxidation processes and changes in the prostanoid levels in the heart. Cardioprotective effect of dalargin during stress may be mediated via peripheral mu and delta opioid receptor stimulation and an inhibition of lipid peroxidation processes through SOD activation and also a recovery, of normal prostanoid levels in the heart.

Animals↗
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[The interaction of mu-opioid receptors with intracellular signal systems].

Review is devoted a modem state of researches of micro-opioid receptor. It is discussed literature data on the integration of micro-opioid receptor with adenylyl cyclase, phospholipase A2, C and D. It is analyzed reports on the interaction of micro-opioid receptor with NO-synthase and guanylyl cyclase.

Adenylyl Cyclases↗
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[Contribution of the endogenous opioid system to regulation of heart resistance to the arrhythmogenic effect of short-term ischemia and reperfusio].

Preliminary selective blockade of micro, delta1, delta2, kappa1, and kappa2 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.

Animals↗
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[The effect of stimulation of cardiac delta1-opioid receptors on the resistance of isolated heart to the action of ischemia and reperfusion].

Preliminary stimulation of cardiac delta1-opioid receptors by DPDPE addition at a concentration of 0.1 mg/liter to the perfusion solution decreased the incidence of reperfusion arrhythmias and the reperfusive destruction of cardiac cells. At the same time, the activation of cardiac delta1-opioid receptors resulted in a decrease in myocardial contractility both in the pre-ischemic period and upon restoration of the coronary flow. Pretreatment with naltriondole (a delta-receptor antagonist) or with cyclopiazonic acid (a specific inhibitor of Ca2+ uptake in sarcoplasmic reticulum) completely abolished the antiarrhythmic, cardioprotective, and inotropic effects of DPDPE. It is suggested that the antiarrhythmic, cardioprotective, and inotropic effects of DPDPE is related to the cardiac delta1-opioid receptor activation and Ca2+ transport alteration on the level of sarcoplasmic reticulum.

Analgesics, Opioid↗
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[Comparative study of the antiarrhythmic activity of mu- and delta-opioid receptor agonists during acute cardiac ischemia and reperfusion models in rats].

It has been established that pretreatment with the selective mu-opioid receptor (OR) agonist DALDA (0.1 mg/kg, i.v.) or the selective delta1-OR agonists DPDPE (0.09 mg/kg) and/or (-)-TAN-67 (0.08 mg/kg) has no effect on the incidence of ventricular arrhythmias induced by a 10-min coronary artery occlusion and a 10-min reperfusion in ketamine-anesthetized rats. In contrast, the pretreatment with the selective delta2-OR agonist deltorphin II (0.12 mg/kg) and the proposed delta2-OR agonists deltorphin D (0.3 mg/kg) and/or dermorphin H (0.23 mg/kg) increases cardiac resistance to the arrhythmogenic action of acute ischemia and reperfusion. Administration of the mixed mu- and delta-OR agonist dalargin (0.12 mg/kg) 15 min before the coronary artery ligation abolished only the reperfusive ventricular fibrillation. It is concluded that peptidergic stimulation of delta2-ORs can be used as a new means of increasing cardiac tolerance to the arrhythmogenic effects of acute ischemia and reperfusion.

Animals↗
PubMedDate not supplied

[The interaction of mu-opioid receptors with ion channels and G-proteins].

The state-of-the-art in investigations of the mu-opioid receptors (ORs) is reviewed. Published information on the interaction between mu-ORs and various G-proteins is summarized and data on the neutral antagonists and inverse agonists of mu-opioid receptor are generalized. The notions about the spontaneous activation of mu-ORs are considered and numerous reports on the interaction between mu-ORs and GIRK, KATP, and Kv channels are analyzed. The role of L, N, and P/Q types of Ca(2+)-channels in mu-OR-mediated intracellular signaling is discussed.

Animals↗
PubMedDate not supplied

[Antiarrhythmic properties of opioid receptor agonists].

Data on the antiarrhythmic properties of opioid receptor (OR) agonists have been systematized. An analysis of published works which indicate that opioids increase cardiac tolerance to arrhythmogenic influences both in vivo and in vitro has been performed. For example, occupancy of central micro- and delta-OR and also ORL1 receptors increases cardiac tolerance to arrhythmogenic action epinephrine and aconitine. In contrast, activation of central kapa-OR exacerbates arrhythmogenic action epinephrine. Stimulation of peripheral delta2- and kappa1-OR decreases an incidence of arrhythmias induced coronary artery occlusion and reperfusion in vivo. Occupancy of peripheral micro-, kappa2-, delta1-OR and also ORL1 receptors has no effect on the cardiac tolerance to arrhythmogenic action of ischemia and reperfusion but increases cardiac electrical stability in rats with post-infarction cardiosclerosis. Authors suggest that opioids which unable penetrate to blood barrier may be used for therapy of arrhythmias.

Animals↗
PubMedDate not supplied

[Adaptation of myocardium to ischemia. The early phase of ischemic preconditioning].

It has been systematized modem data on the early phase of ischemic preconditioning and cardiac resistance to pathogenic action of ischemia and reperfusion. It has been performed an analysis published works on the important role of alteration of myocardium energy metabolism in the development of adaptation resistance of the heart to ischemia. It has been shown that adenosine, bradykinin and opioid peptides and also signalling cascade involved phospholipase C and D, protein kinase C, tyrosine kinase and mitochondrial ATP-sensitive potassium channel play a key role in the mechanism of cardioprotective action of ischemic preconditioning.

Adaptation, Physiological↗