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Biomedical subjects

L N Maslov

Publications and source records attributed to L N Maslov.

At least 55 records · Page 3Linked to original sources
PubMed1999

[Dependence of the pump function of the isolated rat heart on the functional activity of sigma receptors during reperfusion].

Pre-treatment of the sigma-receptor with the sigma-receptor agonist (+)-SKF 10.047 improved the reperfusion recovery of cardiac pump function. The sigma-receptor activation, among other effects, prevented the reperfusion contracture, increased pressure in the left ventricle, and improved survival of cardiomyocytes after ischemia/reperfusion. Pre-treatment with the sigma-receptor antagonist DuP 734 augmented the reperfusion systolic dysfunction of the myocardium and prevented postischemic contractures and cardiac cell lesions. Activation of the cardiac sigma-receptor seems to prompt an augmentation of tolerance to the reperfusion damage.

Animals↗
PubMed1998

[mu-Opiate receptor activation and increase in heart resistance to ischemic and reperfusion injury].

Stimulation of mu-opioid receptors was found to contribute to prevention of myocardial contractile dysfunction and ventricular arrhythmias in ischemia and reperfusion of the rat isolated heart. Endogenous agonists of the mu-opioid receptors were not involved in tonic regulation of the heart resistance against reperfusion disturbances of the rhythm and contractility. On the other hand, mu-opioid receptors are important for development of postischemic contracture.

Animals↗
PubMed1998

[Delta-opiate receptors and heart resistance to arrhythmogenic factors].

Stimulation of peripheral delta-opioid receptors exerted no effect on arrhythmias, whereas that central delta 1- and delta 2-receptor activation decrease the heart susceptibility to arrhythmogenic action of epinephrine. Pre-treatment with the delta-opioid receptor antagonist ICI 174 prevented the antiarrhythmic effect of the central delta-receptors stimulation. The findings suggest that the heart decreased vulnerability to epinephrine-induced arrhythmias following the central delta-receptors stimulation is mediated by an enhanced vagal activity.

Animals↗
PubMed1998

[Modulation of the antiarrhythmic effect by endogenous opioids during adaptation to hypoxia in rats].

Adaptation of rats to hypoxia increased the heart resistance against arrhythmogenic effects. The Met-enkephaline-Arg6-Phe7 contant increased in the hypothalamus of the adapted animals. The blockers of mu- and delta-opioid receptors reduced the antiarrhythmic effect of the adaptation, whereas chi-receptor inhibitor, nor-binaltorphimine, completely abolished it. The findings suggest the antiarrhythmic effect depends on an increase of the endogenous opioids level and modulated effect of these peptides upon autonomous nervous system.

Adaptation, Physiological↗
PubMed1998

[The role of peripheral and central mu-opiate receptors in the modulation of adrenergic cardiac lesions during stress].

Immobilisation stress-induced heart damage in rats. Pretreatment with guanethidine decreases myocardial catecholamine level and completely reverses cardiac injury induced by stress. Bretylium eliminates norepinephrine release from sympathetic nerve terminals in myocardium and decreases stress-induced heart damage. Activation of peripheral mu-opioid receptors abolishes the stress-induced cardiac injury and increases endogenous myocardial and adrenal catecholamine level). The findings suggest that the stress-induced cardiac lesions depend on activation of the sympatho-adrenomedullary system whereas the endogenous mu-receptors agonists modulate heart resistance against stress-induced damages).

Adrenal Glands↗
PubMed1997

Participation of central kappa-opioid receptor in arrhythmogenesis.

The effect of kappa receptors agonists and antagonists was studied in the model of epinephrine induced arrhythmias. Kappa receptor agonists U-50,488 and [D-Ala2]-Dynorphin A (1-13) administered I.C.V. potentiate the arrhythmogenic effect of epinephrine. The effect of U-50,488 was completely blocked by kappa receptor antagonist, nor-binaltorphine. Administration of N-cholinergic receptor inhibitor, hexamethonium, prevented pro-arrhythmic effects of U-50,488 and [D-Ala2]-Dynorphin A (1-13). The data support the hypothesis that central kappa opioid receptors play an important role in the arrhythmogenesis.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1997

[Heart resistance against stress-induced damages].

Activation of peripheral-opioid receptors diminished stress-induced heart damage whereas stimulation of central-opioid receptors enhanced it. Peripheral-opioid receptors do not take part in pathogenesis of the "stress cardiomyopathy". The prostanoid system and processes of lipid peroxidation participate in realisation of cardioprotective effects associated with peripheral-opioid receptors.

Animals↗