[Participation of heart prostaglandins in cardioprotective cross-effects of adaptation to stress and hypoxia].

An adaptation to stress and hypoxia was found to increase the baseline PGE content in the myocardium. The data obtained suggest that the activation of the myocardial system of protective PGs is an important link in the cardioprotective effects of adaptation.

[The role of the inositol phosphate cycle in the cardioprotective effect of adaptation to repeated stressors].

As shown by previous studies, adaptation to short-term stress exposure developed the phenomenon of adaptive stabilization of structures (PhASS), including such as elevation in resistance to impairing effects of isolated animal hearts and the heart nuclear fraction of elements of the sarcoplasmic reticulum. Studies of the role of inositol phosphate regulatory cycle in the development of the ASS phenomenon showed that the inositol triphosphate-diacyl glycerol (ITP-DAG) step of regulation was activated at the peak of PhASS development within 15 days after the adaptation onset. The activation observed was accompanied by enhanced activity of phospholipase C as well as by positive inotropic responses of heart tissue to phenylephrine stimulation, which was determined by ITP and DAG accumulation.

[Role of the inositol phosphate cycle in the cardioprotective effect of adaptation to intermittent hypoxia].

The impact of adaptation to intermittent hypoxia of different duration (for 20 and 40 days) on the inositol triphosphate-diacylglycerol (ITP-DAG) regulatory contour in the heart was investigated. For this, isolated heart alpha 1-adrenoreactivity to phenylephrine and phospholipase (PhL-C) activities were studied in cardiac plasma membranes. On day 20 of adaptation, the heart inotropic response to phenylephrine stimulation was somewhat reduced and the activity of Ca(2+)-dependent PhL-C did not differ from that in the controls within the range of Ca2+ physiological concentrations.

[The role of the prostaglandin system in the cardioprotective effect of adaptation to hypoxia in stress].

The adaptation to periodic altitude hypoxia is known to have cardioprotective and antiarrhythmic effects in stress-induced and ischemic lesions. The effects are assumed to be associated with the enhanced activity of the body's stress-limiting systems, including prostaglandins (PG). Wistar rats were adapted in a hypobaric chamber at an altitude of 4000 m for 6 hours during 40 days.

[Increase of calcium-dependent activity of phospholipase C in the myocardium in adaptation of animals to short-term stress effects].

The effect of adaptation of rats to repeated short-term stress exposures was studied on the density and the affinity of alpha 1-adrenoceptors in the heart and on the phospholipase C activity and sensitivity to changes in Ca2+ concentration. It was found that adaptation to stress was accompanied by a desensitization of alpha 1-adrenoceptors and also by an increase in Ca(2+)-dependence of phospholipase C activity in the heart. The role of increased activity of phospholipase C and activated inositol triphosphate-diacylglycerol regulatory cascade is discussed as regard to the previously revealed accumulation of heat shock proteins in the myocardium and to the adaptive protection of the heart.

[Increase of alpha 1-adrenoreactivity of the rat heart in adaptation to periodic hypoxia].

There is a possibility that the cardioprotective effect of adaptation to intermittent hypoxia is due to changes in receptors apparatus of the heart. In this connection the effect of preliminary adaptation to intermittent hypoxia (4 hours per day at the altitude of 4000 m during 40 days) on the state of beta-receptors-adenylate-cyclase system and same other receptors of the heart were studied. It was shown that at the end of the course of adaptation the number of beta-adrenoceptors in the heart was increased with simultaneous decrease in basal adenylate-cyclase activity, accompanied by the diminution of its response to beta-agonist.

[Effect of adaptation to periodic hypoxia on the resistance of the indicators of energy metabolism and myocardial contraction in acute anoxia and reoxygenation].

The effect of preliminary adaptation to intermittent (40 days, 4 hrs daily at 4000 m "altitude") on the resistance of myocardial energy metabolism and contractile function to acute anoxia and subsequent reoxygenation was studied. It was found that adaptation to hypoxia significantly accelerated the restoration of creatine phosphate, ATP and creatine phosphokinase activity in myocardium in reoxygenation following acute anoxia. On the whole, this effect reduces the competition of H+ with Ca2+ in myofibrils to improve the energy supply and to accelerate the restoration of myocardial contractile function in reoxygenation.

[Alpha1 desensitization of the heart during adaptation to stress].

Results of the experiments evidence that a combination of three factors, limiting the Ca2+ concentration increase in myocardial cell, can play a role in the cardioprotective effect of adaptation of rats to short-term immobilization stress (every second day for a month) are presented. Those factors are as follows: desensitization of alpha 1-adrenoreceptors, M-cholinoreceptors up-regulation and reduced number of voltage-dependent Ca2+ channels in the myocardial membranes.

[Effect of ionol on carcinogenesis in the kidneys].

The effect of treatment with an antioxidant--ionol (2,6-di-tert-butyl, 4-methylphenol)--on nitrosodimethylamine-induced carcinogenesis was studied. Large doses of ionol were found to inhibit tumor development in the kidney. This also involved intensification of spontaneous peroxidation of renal cortical membrane cell lipids which in turn was inhibited when additional stimulation with iron was carried out.

[Immune and hormonal response to dimethylnitrosamine].

The study was concerned with assay of levels of 11- HOCS in blood and adrenal tissues and antibody-producing cells in the spleen as well as spontaneous rosette-formation by blood thymic and splenic lymphocytes in the course of carcinogenesis induced in experimental animals by nitrosodimethylamine treatment. Heightening of adrenal cortical function was registered at two stages: at an early stage of carcinogenesis--two months after nitrosodimethylamine treatment, and during tumor progression--after 7 months. Cellular immunity inhibition was observed at the said periods.