[Morphofunctional manifestations of cardioprotective effect of mu-opioid receptor stimulation in stress]. / Morfofunktsional'nye proiavleniia kardioprotektornogo éffekta stimuliatsii mu-opiatnykh retseptorov v usloviiakh stressa.

Activation of peripheral mu-opioid receptors contributes to an increase in stability of cardiomyocytes to stress damage manifesting with decreased accumulation of Tc-99m pyrophosphate in the heart muscle and contractures of the myocardium. As a principal mechanism of mu-receptor-dependent increase in resistance of the heart to stress damage, modulated influence of opioids on adrenergic pathogenetic links of heart stress damage is considered. In realization of the discovered cardioprotective effect associated with mu-receptor activation, opioidergic limitation of histamine release from mast cells in the myocardium and also mu-receptor-dependent intensification of coronary bloodstream in stressed animals may play a definite role.

[Interrelations between sympathetic adrenal and opioid systems--regulatory mechanism determining cardiac resistance to stress damage]. / Vzaimodeistvie simpatoadrenalovoi i opioidnoi sistem kak reguliatornyi mekhanizm, opredeliaiushchii ustoíchivost' serdtsa k povrezhdaiushchemu deistviiu stressa.

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.

[The role of peripheral and central mu-opiate receptors in the modulation of adrenergic cardiac lesions during stress]. / Rol' perifericheskikh i tsentral'nykh mu-opiatnykh retseptorov v moduliatsii adrenergicheskogo povrezhdeniia serdtsa pri stresse.

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).