[Opposite effects on antioxidant enzymes of adaptation to continuous and intermittent hypoxia]. / Protivopolozhnoe vliianie adaptatsii k nepreryvnoi i periodicheskoi gipoksii na antioksidantnye fermenty.

Adaptation to continuous hypoxia under mid-mountain conditions (altitude 2100 m) decreases the content of lipid peroxidation products and the activity of superoxide dismutase and catalase in rat heart, liver, and brain, with a concomitant decline in the resistance to reperfusion arrhythmias. On the contrary, adaptation to intermittent hypoxia in the altitude chamber increases the activity of the antioxidant enzymes in the same organs, while the content of peroxidation products remains normal; at the same time, the heart becomes more resistant to reperfusion arrhythmias. The mechanism is discussed that ensures enhanced antioxidant protection in adaptation to intermittent hypoxia.

[Effects of adaptation to periodic hypoxia on Ca2+ pump of the cardiac sarcoplasmic reticulum and its resistance to endogenous damaging factors]. / Vliianie adaptatsii k periodicheskoi gipoksii na Ca2+-nasos sarkoplazmaticheskogo retikuluma serdsa i ego ustoichivost' k éndogennym povrezhdaiushchim faktoram.

The adaptation of rats to periodic "altitude" hypoxia in the altitude chamber (6 hour daily at an altitude of 5000 m during a month) led to increased activity of the Ca2+ pump in the myocardial sarcoplasmic reticulum, which was associated with lower Kd values and higher calcium transport Vmax. When a cardiac homogenate was kept at 4 degrees C, autolysis resulted in a decrease in Ca2+ pump activity (which was more rapid in adapted animals than in the controls) and an equal increase in the levels of free calcium in the homogenates in the two series of experiments. The approximate data were obtained when a homogenate was incubated at 37 degrees C, but when it was incubated at 4 degrees C, the rate of Ca(2+)-pump inactivation decreased 20-fold. Incubation in the presence of free radical oxidative inductors (Fe2+ ascorbate) led to high resistance of myocardial Ca(2+)-pump in the adapted rats. The paper discusses the causes of myocardial Ca(2+)-pump activation in periodic hypoxic adaptation and the mechanisms for its increased resistance to active oxygen, as well as their role in the cardioprotective effect of the adaptation.

[The effect of surgical stress on DNA synthesis in liver and brain cells]. / Effekty operatsionnogo stressa na sintez DNK v kletkakh pecheni i mozga.

Distinct alterations in the rate of DNA synthesis (an increase in the rate of reparation and a decrease in the rate of replication in nuclei and mitochondria) were detected in liver and brain cells during the stress caused by surgical operation. Within 8-10 hrs after the operation the rate of DNA reparation was increased by 40-50% in nuclei of liver cells and by 31-35% in brain cell nuclei. Replication of nuclear DNA was decreased immediately after the operation--by 33% in liver cells and by 50% in brain cells. Within a day after the operation the rate of replication was restored up to the control level in liver cells, while it was still decreased by 30% in brain cells. The rate of mitochondrial DNA synthesis was slightly decreased within the first 12 hrs after the operation: by 12-14% in liver cells and by 18-20% in brain cells. The stress, and particularly postoperative stress, exhibited pronounced action on structure and various systems of DNA synthesis in cells of various tissues.

[Suppression of replication and activation of DNA reparative synthesis in stress and prevention of these phenomena by preliminary adaptation]. / Podavlenie replikatsii i aktivatsiia reparativnogo sinteza DNK pri stresse i preduprezhdenie étikh iavlenii predvaritel'noi adaptatsiei.

Effects of preliminary adaptation to short-term stress or to regular hypoxia on disturbances of DNA biosynthesis were studied in liver and heart tissues under conditions of emotional-painful stress (EPS). EPS was found to induced activation of DNA reparative synthesis in heart and liver tissues and affected dissimilarly DNA replication in these tissues: activation of the reaction in heart and suppression in liver tissue. Adaptation to regular hypoxia limited distinctly the burst of DNA reparative synthesis in cells of both these tissues, reduced activation of the DNA replicative synthesis in heart and prevented the stress induced depression of DNA replication in hepatic cell nuclei and mitochondria. Mechanisms of the hepatoprotective effect of adaptation to hypoxia is discussed.

[DNA synthesis in heart cells in its compensatory hyperfunction]. / Sintez DNK v kletkakh serdtsa pri ego kompensatornoi giperfunktsii.

In modelling compensatory hyperfunction of the heart (CHH) due to coarctation of the aorta, the replication rate in the nuclei of myocardial cells increases in 24 hours and becomes 20 fold the control values in 48 hours. The replication rate in myocardial mitochondria in CHH reduces at the beginning of hyperfunction but increases almost two fold in 48 hours. The DNA reparation rate in the nuclei of the myocardial cells does not change in CHH. The rate of this process, however, increases significantly (by 50-74%) in cardiac cells of animals subjected to operation but without coarctation of the aorta.

[Effect of adaptation to continuous and intermittent hypoxia on heart resistance to ischemic and reperfusion arrhythmias]. / Vliianie adaptatsii k deistviiu nepreryvnoi i periodicheskoi gipoksii na rezistentnost' serdtsa k ishemicheskim i reperfuzionnym aritmiiam.

The effect of adaptation to intermittent hypoxia in a pressure chamber (5.000 m daily for 6 hours for 30 days) on arrhythmias occurring in occlusion of the coronary artery and subsequent reperfusion in rats was compared with the effect of adaptation to continuous hypoxia at middle-mountain altitudes. Adaptation to intermittent hypoxia reduced the duration of severe ventricular arrhythmias in acute ischemia and reperfusion to a great measure. Adaptation to continuous hypoxia at middle-mountain altitudes has a similar effect only in ischemic arrhythmias but at the same time promotes the development of reperfusion arrhythmias. The possible mechanisms of these effects are discussed.

[Elimination of stress-induced activation of DNA reparative synthesis in the myocardium by increasing the load on the heart]. / Ustranenie stressornoi aktivatsii reparativnogo sinteza DNK v miokarde posredstvom uvelicheniia nagruzki na serdtse.

The rate of DNA reparative synthesis was studied in the nucleus of myocardial cells in the heart compensatory hyperfunction (HCH) induced by the aorta coarctation and in animals exposed to surgical stress without the aorta coarctation. It was established that both surgery and emotional painful stress activated the DNA reparative synthesis in myocardial cells. For example, 12-24 hrs following the surgery the DNA reparation rate exceeded control values by 50-74%. HCH induced no changes in the DNA reparation rate in nuclei of myocardial cells. The mechanism of stress-induced DNA damage is discussed and a hypothesis is put forward on stabilizing the effect of hyperfunction on the DNA structure.

[The effect of emotional-pain stress on the rate of DNA synthesis in heart and liver cells]. / Vliianie émotsional'no-bolevogo stressa na skorost' sinteza DNK v kletkakh serdtsa i pecheni.

Effect of a single long-term (6 hrs) emotional-painful stress on DNA synthesis was studied in nuclei and mitochondria of heart and liver cells. Various systems of DNA synthesis in heart and liver cells were shown to respond dissimilarly to the stress. The rates of replication and reparative synthesis of nuclear DNA were increased while synthesis of mitochondrial DNA was unaltered in heart cells within the first day after the stress. In liver cells the reparative synthesis of nuclear DNA was also increased, whereas the rate of its replication in nuclei and mitochondria was distinctly inhibited for a long time. Thus, the systems of DNA synthesis in liver cells proved to be more sensitive to extreme stress-reactions as compared with heart cells. Effect of the stress on the systems of DNA synthesis in specific and connective tissue cells of liver and heart is discussed. At the same time, mitochondria are localized in specialized cells of both heart and liver tissues. The data obtained suggest that inhibition of the mitochondrial DNA synthesis is realized in hepatocytes.

[Comparative evaluation of the effect of vitamin E deficiency on lipid peroxidation and Ca2+ transport in heart and skeletal muscles]. / Sravnitel'naia otsenka vliianiia nedostatochnosti vitamina E na perekisnoe okislenie lipidov i transport Ca2+ v serdechnoi i skeletnoi myshtsakh.

10-fold decrease of alpha-tocopherol content in blood serum, distinct increase in hemolysis of erythrocytes and activation of lactate dehydrogenase in blood plasma were found in rats kept on a vitamin E deficient diet within 2 months as compared with control. Content of alpha-tocopherol was decreased in myocardium 3.4-fold and in skeletal muscles--5.4-fold. Lipid peroxidation was activated in myocardium and skeletal muscles under conditions of vitamin E deficiency. Content of diene conjugates and Schiff bases was increased by 30-60% in these tissues; content of malonic dialdehyde--the secondary product of lipid peroxidation--was increased in myocardium by 60% and in skeletal muscles--4-fold. Activity of lysosomal enzymes was altered only slightly in myocardium, whereas in skeletal muscles unsedimented activity of acid phosphatase was distinctly increased. The activation of impairing factors observed led to deterioration of Ca2+ transport functions of membranes in myocardium by 30% and in skeletal muscles--4-fold. The data obtained suggest that heart muscle is better protected against vitamin E deficiency as compared with skeletal muscle. Physiological importance of these results is discussed.

[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 the activation of lipid peroxidation and of damage to the myocardial antioxidant systems in stress and experimental infarct]. / Preduprezhdenie aktivatsii perekisnogo okisleniia lipidov i povrezhdeniia antioksidantnykh sistem miokarka pri stresse i éksperimental'nom infarkte.

It was shown that the multifold increase of intermediate products of lipids peroxidation, their hydroperoxides, and terminate products of this process, Shiff's bases, occurred in rats with experimental myocardial infarction both in the ischemic and in nonischemic zones. Simultaneously the activity of antioxidant enzymic systems reduced in the myocardium; the superoxydismutase and catalase activities decreased insignificantly and the glutatione peroxidase activity was 2-fold decreased. The preliminary adaptation of the animals to the periodic action of hypoxia itself did not influence the antioxidant systems of the organism but it significantly decreased the accumulation of the lipids peroxidation products and the size of ischemic necrosis. It is suggested that the protective effect of the adaptation of hypoxia during the heart ischemic damage is realized not by the increase of the antioxidant systems activity but by the change in the membrane lipid composition.

[Damage to the Ca2+-transport system of cardiac sarcoplasmic reticulum during emotion-pain stress]. / Povrezhdenie Ca2+-transportiruiushchei sistemy sarkoplazmaticheskogo retikuluma serdtsa pri émotsional'no-bolevom stresse.

The influence of emotional-pain stress on the properties of the sarcoplasmic reticulum Ca2+-transporting system of the rat heart muscle was studied. The decrease of the Ca2+-dependent component of the Ca2+, Mg2+-ATPase activity, Ca2+-binding capacity and the rate of Ca2+-transport was found in the animals after stress. These alterations in the Ca2+-transporting system were caused by lipid peroxidation and could be prevented by the antioxidant ionol.

[Inhibition of lipid peroxidation during emotional-painful stress by ionol and gamma-hydroxybutyric acid]. / Ingibirovanie ionolom i gamma-oksimaslianoi kisloti aktivatsii perekisnogo okiosleniia lipidov pri émotsional'no-bolevom stresse.

UV spectroscopy, polarography and fluorescence of Schiff's bases were used to study the time course of emotional pain stress-induced accumulation of the primary and secondary products of lipoperoxidation (LPO) in different tissues of Wistar rats and to appraise the effect of gamma-hydroxybutyric acid (GHBA) and 4-methyl-2,6-ditretbutylphenol (ionol) on LPO induction. LPO activation was shown to be retained after emotional pain stress for a long enough period of time. This activation may last from 2 to 5 days depending on the organ. Pretreatment with GHBA or ionol completely reverses LPO activation.

[Lipid peroxidation activation and the focal contracture injuries in the myocardium under emotional-pain stress]. / Aktivatsiia perekisnogo okisleniia lipidov i ochagovye kontrakturnye povrezhdeniia v serdechnoi myshtse pri émotsional'on-bolevom stresse.

Emotional-pain stress reproduced in the form of so called anxiety-neurosis provokes long-term activation of lipid peroxidation associated with an increased content of its products in the myocardium and the development of focal lesions of the contracture type in myocytes. These heart lesions are likely to be related to the impairment of active calcium release from myofibrils due to lipid hydroperoxides-induced injury to cell membranes responsible for the cation transport. While progressing the morphologic changes in the heart reach maximum, i. e. lead to complete contracture and necrosis of myocardial cells.

[Activation of lipid peroxidation in emotional-pain stress]. / Aktivatsiia perekisnogo okisleniia lipidov pri émotsional'no-bolevom stresse.

Accumulation of primary and secondary products of lipid peroxidation (PLP) in different tissues of Wistar rats under emotional-pain stress (EPS) was studied using UV-spectrophotometry and fluorescense of Schiff bases. It was shown that under EPS the amount of PLP increased mostly in the heart and to a lesser degree in the skeletal muscle and brain. An increase in hydroperoxidases in all the organs studied was less than that in the PLP end-products, i. e. flourescent Schiff bases.