[Myocardial contraction in the reverse development of adaptation to short-term exposure to stress].

Contractile function of an isolated right atrium was studied in short-term stressor effects-adapted male Wistar rats at different times after adaptation was completed. Adaptation to short-term stressor effects was shown to produce a restricted decrease of myocardial contractility shortly after adaptation was completed. At the 3d day another decrease of contractile function was noted.

[Age-related characteristics of poststress DNA repair in the myocardium].

It has been demonstrated that young and adult rats had age-associated differences in stress-induced lesions and in poststressor repair of DNA synthesis in the myocardium. In both age groups, the DNA repair systems perform an identical scope of work aimed at abolition of poststressor lesions with the difference that in young rats, the repair is completed 2 days and in adult rats 3 days after exposure to stress is discontinued.

[Effect of interferon and its liposome-incorporated inducer on the recovery of natural killer activity after immobilization stress].

In this work the data on the decrease of the activity of natural killer cells, determined in the test of the release of radioactive chromium from labeled target cells YAC-1 in CBA and BALB/c mice after stress caused by 6-hour immobilization, are presented. The use of mouse leukocyte interferon and the agents inducing its synthesis (double-helical RNA and poly I X poly C, especially poly I X poly C contained in liposomes) has been shown to be highly effective for the restoration of the activity of natural killer cells after its suppression at the period following the stress. The probable role of deficiency of interferon-inducing agents in the mechanisms of decrease of natural cell-mediated cytotoxicity after stress is discussed.

[Interrelations of natural cellular cytotoxicity and interferon systems in immobilization stress].

The suppressed cytotoxic natural killer activity was observed in the mouse spleen during 2 days after 6 h of immobilization stress. Both serum interferon level and interferon production by spleen cells under PHA, ConA and enterotoxin stimulation were also significantly decreased. The period of suppression was followed by the recovery of the activity of the two systems by day 7-9.

[Lipid peroxidation in experimental myocardial infarct: the action of hyperbaric oxygenation].

Rats with experimental myocardial infarction demonstrated decrease in the activity of superoxide dismutase and catalase and increase in the content of lipid peroxidation (LPO) products and Schiff bases both in and outside the area of necrosis. The combined ischemic damage and hyperbaric oxygenation resulted in the over additive effect of accumulation of LPO products in and outside the area of infarction. The data suggest that it is desirable to use antioxidants during hyperbaric oxygenation.

[Prevention of heart contractile disorders in experimental infarct by using preliminary adaptation to stress exposure and opioid peptides].

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.

[Comparative evaluation of stress-induced depression of normal killer activity in old and young animals and its elimination by interferon].

The data are presented on the comparative evaluation of a poststress decrease in the activity of normal killer cells, determined in the test of the release of 41Cr from target cells YAC-1 in young and old CBA mice after 6-hour immobilization. The use of mouse leukocyte interferon and poly I . poly C acid has been shown to be highly effective for the restoration of the activity of normal killer cells in young animals after its stress-induced suppression, while in old animals these immunomodulators have proved to be considerably less effective in restoring the activity of natural killer cells at the period following the stress.

[Phenomenon of post-stress rigidity in the left ventricular myocardium].

The effect of emotional painful stress on myocardial distensibility and contractility was studied on an isolated papillary muscle of the rat left ventricle. The EPS resulted in decreased distensibility and depressed amplitude of papillary muscle contraction. These disturbances are suggested to play the main role in the development of heart insufficiency under stressful situations.

[Changes in cardiac contractile function in the dynamics of emotional-pain stress].

Emotional painful stress provokes phasic disorders of heart contractile function, the time course of which corresponds to the temporary parameters of the phasic development and to the recovery of the metabolism and structure of the heart.

[Prevention of disorders of myocardial contractile function under stress by the preliminary adaptation of animals to physical load].

Rats adapted to exercise (daily swimming for one hour over 30 days) and control animals were subjected to emotional-painful stress (EPS) according to the pattern of anxiety neurosis. It has been established that EPS decreases the amplitude as well as the rate of contractions and relaxations of the isolated papillary muscles of animals by 2-3 times and also reduces the resistance of the contractile function of the myocardium to the excess of Na+ and H+ ions, ousting Ca2+ from the sites of its binding in the sarcolemma. Adaptation to exercise exerts an opposite effect.

[Role of lipid peroxidation in the pathogenesis of arrhythmias and the anti-arrhythmogenic action of antioxidants].

In the initial phase of its action on the contracting myocardium the inductor of lipid peroxidation (LPO) H2O2 displays marked positive ino- and chronotropic as well as relaxant effects which are, therefore, close to catecholamine effects. Since catecholamines activate LPO it suggests that such activation may be involved in the mechanism of their physiologic action. The prolongation of H2O2 action inevitably leads to the development of bradycardia and bradyarrhythmic arrhythmia which may ultimately end in cardiac arrest.

[Increased brain Na, K-ATPase activity of rats under stress].

The activities of Na, K- and Mg-dependent ATPases were measured in crude synaptosomal fractions isolated from the rat brain gray matter. Prolonged (6 h) exposure to emotional painful stress stimulated Na, K-ATPase activity by 40% without affecting that of Mg-ATPase. Preliminary injection of the free radical scavenger ionol presented Na, K-ATPase activation, thus suggesting the involvement of lipid peroxidation initiated in brain tissues under stress in acceleration of NA-pump function.

[Disorders of contractile function and adrenoreactivity of the portal vein in emotionally-painful stress and experimental myocardial infarct and their prevention by means of membrane protectors].

The effect of emotional-painful stress (EPS) and experimental myocardial infarction on portal vein contractile function, adrenoreactivity , and resistance to the glucose shortage was studied on the rat. The myocardial infarction was shown to result in shifts of the smooth muscle contractile function which were similar to those in EPS, though being somewhat less pronounced. These changes included depressed spontaneous contractility, reduced adrenoreactivity and decreased resistance to the shortage of glucose in the washing solution.

[DNA damage and reparative synthesis in various organs of the rat, induced by emotional-painful stress].

Emotional-painful stress results in DNA single-strand breakage and repair synthesis activation in all the organs studied. The process is tissue-specific.

[Age-related dynamics of the contractile function of the myocardium and its relation to cardiomyocyte size].

An experimental study in rats has demonstrated that age-related decrease in basic contractility parameters of the heart muscle shows correlation with an increase in the volume of cardiomyocytes making up the muscle and a reduction of specific area under these cells' sarcolemma. Functional depression grows with age, so does heart response to changed calcium concentration in bath medium, and positive inotropic effect of high-frequency stimulation and adrenoreactivity are enhanced. Since these effects are mediated by calcium influx into the myocyte, their enhancement can be related to the fact that the capacity of sarcolemmal transport systems responsible for calcium withdrawal from the cells grows weaker with age.

[Disorders of the heart contractile function in chronic hemolytic anemia and their prevention].

The coronary blood flow and heart contractile function were studied on rats with phenylhydrazine-induced chronic hemolytic anemia. The coronary blood flow in the animals' hearts was increased 2.5-fold, whereas the main parameters of contractile function were reduced but insignificantly.

[Comparative evaluation of the myocardial resistance of animals with hereditary hypertension and normal arterial pressure to the damaging action of stress].

In normotensive WKY and August rats the 6-hour immobilized stress has been shown to result in decrease of heart muscle extensibility, in depression of developed tension and reduction of myocardial resistance to hypoxic and calcium contractures. This complex does not develope the post-stress disturbances of miocardial function in spontaneously hepertensive rats (SHR) which heart muscle is characterized by reduced adrenoreactivity. The heart adrenoreactivity is supposed to be one of the important factors determining its resistance to stress damage in animals of different strains.