[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).