[Effect of stress, infarction and adaptation to brief exposure to stress on opioid peptide levels in the brain]. / Vliianie stressa, infarkta i adaptatsii k korotkim stressornym vozdeistviiam na soderzhanie opioidnykh peptidov v golovnom mozge.

Content of beta-endorphine, Met- and Leu-encephalines was studied in various brain regions and in adrenal glands after long-term immobilization stress, after myocardial infarction and during prolonged gradual adaptation to short-term stressory affects. Acute stressory conditions, myocardial infarction or, especially distinct adaptation to short-term stressory affects were shown to cause an accumulation of opioid peptides in brain structures and in adrenal glands. This increase in opioid peptides accumulated as a tissue reserve appears to elevate the body resistance to subsequent injuring affects.

[Prevention of disorders in the contractile function of non-ischemic sections of the heart during experimental infarction using beta-endorphin]. / Preduprezhdenie narushenii sokratitel'noi funktsii neishemizirovannykh otdelov serdtsa pri éksperimental'nom infarkte s pomoshch'iu beta-éndorfina.

The effect of pretreatment with beta-endorphin on disorders of right-atrial myocardial distensibility and contractility in left-ventricular infarction (by Selye) was examined in Wistar rats. This peptide, administered intravenously (50 micrograms/kg) immediately before the simulation of infarction, was shown to reduce considerably infarction-induced impairment of distensibility and contractility of an isolated right atrium and of its resistance to hypoxia and excessive calcium, and also to increase the survival rate. The results of the study suggest that the protective effect of beta-endorphin is chiefly due to its central action.

[Prevention of disorders in the contractile function of the nonischemic portion of the heart during infarction by preliminary adaptation to brief stress exposures]. / Preduprezhdenie narushenii sokratitel'noi funktsii neishemizirovannogo otdela serdtsa pri infarkte s pomoshch'iu predvaritel'noi adaptatsii k korotkim stressovym vozdeistviiam.

Preliminary adaptation to short-term exposures to immobilization stress prevents to a large extent the depression of contractile function and the lowering of the right atrium myocardium resistance to hypoxia and excess Ca2+ in experimental infarction of the left ventricle. This fact agrees with the concept that disturbance occurring in the nonischemic heart during infarction is caused by stress-induced damage.

[Limitation of disorders of the contractile function of the nonischemic areas of the myocardium during infarct by using the delta-sleep peptide and its cyclic derivative]. / Ogranichenie narushenii sokratitel'noi funktsii neishemizirovannykh otdelov miokarda pri infarkte s pomoshch'iu peptida del'ta-sna i ego tsiklicheskogo proizvodnogo.

The effect of pretreatment with delta-sleep peptide (DSP) and its cyclic analogue (cDSP) on right-atrial myocardial distensibility and contractility disturbances in left-ventricular infarction (according to Selye) was studied in Wistar rats. These peptides, administered in a 20 micrograms/kg dose, 1 hour before the induction of experimental infarction, significantly limited the infarct-related depression of atrial distensibility and contractility, and also reduced atrial resistance to hypoxia and excessive calcium. Since infarction-associated disorders of myocardial structure and function in non-ischemic regions of the heart are due to the emotional-painful stress that accompanies the infarction, it can be assumed that the protective effect of DSP and cDSP consists in limiting the stress-induced response.

[Prevention of heart contractile disorders in experimental infarct by using preliminary adaptation to stress exposure and opioid peptides]. / Preduprezhdenie narushenii sokratitel'noi funktsii serdtsa pri éksperimental'nom infarkte s pomoshch'iu predvaritel'noi adaptatsii k stressovym vozdeistviiam i opioidnykh peptidov.

Preliminary adaptation to brief immobilization stresses was shown to reduce impairments of the contractile function of the left ventricle in an experimental myocardial infarction both under conditions of physiological rest and following the short blocking of the aorta. This protective effect is occasioned, along with other factors, by the prevention of the stressory damage to the non-ischemic portions of the heart. The same adaptation increased the levels of enkephalins and beta-endorphin in the cerebral and adrenal structures. The preliminary administration of beta-endorphin prior to the stimulation of an experimental infarction considerably prevented stressory disorders of the contractile function of the right atrium.