[Prognostic value of the content of lipid peroxidation products in tissues at pancreatic necrosis].

The exact role of lipid peroxidation in pathogenesis of pancreatonecrosis was established by means of studying the level of dienic conjugates and malonic dialdehyde in the intraoperative bioptates of the pancreas, liver, lymph nodes of the lesser omentum in 40 patients as well as in the autopsy material (similar tissues, spleen and bone marrow) in 18 patients dead of destructive pancreatitis. The control group included 10 patients dead of sudden death (normal), group of comparison (those who died of acute myocardium infarction--10 subjects) and of acute surgical abdominal pathology not associated with pancreatitis (10 subjects). Demonstrable activation (6-10 times) of processes of lipid peroxidation in all the bioptates under study took place at pancreatonecrosis as compared to the normal that suggests generalization of lipid peroxidation at this pathology.

[The body's responses to extreme exercise: biochemical aspects].

Experiments on animals and clinical studies in athletes have shown a negative impact of extreme exercises on the physicochemical characteristics of biomembranes. The resultant decrease in the activity of different isoforms of the multienzymatic system of hepatic cytochrome P450 may underlie, firstly, the formation of a vicious circle of increases in the microviscosity of biomembranes and membrane-dependent processes and, secondly, the lowered resistance of athletes to chemical environmental factors, which should be borne in mind during the professional activity of high-class athletes.

[Experience in treating patients with cardiovascular diseases by means of adaptation to periodic barochamber hypoxia].

Adaptation to periodic hypoxia (decompression 490 mm Hg) in a multiplace medical pressure chamber of patients with hypertension, cardial neurocirculatory asthenia, coronary heart disease produced a persistent hypotensive effect with improvement of central and peripheral hemodynamics, oxygen homeostasis, electrolyte balance of blood. In patients with neurocirculatory asthenia associated with ventricular and supraventricular extrasystole positive hemodynamic changes accompanied a persistent antiarrhythmic effect. In addition to the latter, CHD patients experienced improvement in myocardial contractility.

[The nondrug treatment of hypertension patients by their adaptation to periodic hypoxia in a barochamber].

Patients with essential hypertension were exposed to periodic hypoxia in a pressure chamber. It is shown that adaptation to periodic hypoxia results in improvement of general condition of patients who exhibited a decline in blood pressure, minute blood volume, serum sodium concentrations as well as better microcirculation and tissue oxygen tension. Reduced concentrations of total serum cholesterol and atherogenic index were achieved in hypercholesterolemia patients.

[Adaptation to periodic hypoxia decreases ethanol consumption and abstinence-related damages to the internal organs during withdrawal in chronically alcoholized animals].

Adaptation to intermittent hypoxia in a hypobaric altitude chamber reduced two-fold ethanol consumption in chronically alcoholized rats and limited or eliminated abstinence syndrome. The effect of the adaptation was evident from prevented development of abstinence analgesia, enhanced alcohol consumption following deprivation, abstinence activation of lipid peroxidation in the liver, and release of hepato-specific enzymes fructose monophosphate and gamma-glutamyl transpeptidase into blood. At the same time adaptation prevented the fall of cardiac fibrillation threshold and pronounced disturbance of ventricular contraction and relaxation.

[The role of the liver macrophage system in decreasing the immune complex level of the blood during adaptation to periodic hypoxia].

It has been established that adaptation to intermittent hypoxia in altitude chamber considerably increases the capacity of hepatic macrophagal systems (MFS) to uptake Indian ink particles from the blood as well as immunoglobulin labelled with fluorescein isothiocyanate. There is simultaneous catabolism of labelled albumin in hepatic MFS. It has been suggested that the increased C3b-component of complement system in blood observed in adaptation to hypoxia plays a substantial role in the activation of hepatic MFS.

[Reversal of withdrawal injuries of the heart and liver by adaptation to intermittent hypoxia when discontinuing ethanol in chronically alcoholized animals].

Adaptation to intermittent hypoxia in the hypobaric altitude chamber showed a two-fold decrease in ethanol consumption in chronically alcoholized rats and attenuated or arrested the withdrawal syndrome. The impact of adaptation to the withdrawal syndrome was that it prevented the development of withdrawal analgesia, higher alcohol consumption after its withdrawal, withdrawal hepatic activation of lipid oxidation products and blood release of the hepatic specific enzymes fructose monophosphataldolase and gamma-glutamyl transpeptidase. Concurrently, the adaptation prevented the withdrawal fall of the cardiac fibrillation threshold and marked disorders of ventricular contraction and relaxation.

[Comparative evaluation of the protective effect of sodium valproate, phenazepam and ionol in stress-induced liver damage in rats].

Ionol, a synthetic antioxidant, limits the stressor liver injury to a greater extent than sodium, valproate and phenazepam, activators of a GABA-ergic link of the stress-limiting organism systems. This injury is exhibited in the organospecific elevated levels of blood enzymes fructosediphosphate aldolase depression of N-demethylase activity of microsomal monooxygenases and a decrease in the amount of cytochromes P-450 and B5.

[Suppression of replication and activation of DNA reparative synthesis in stress and prevention of these phenomena by preliminary adaptation].

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.

[Determination of liver cholesterol-7 alpha-monooxygenase activity in an in vivo experiment].

The method of determination of cholesterol-7 alpha-monooxygenase activity in vivo which has a number of advantages over the existing ones is offered. [3H]cholesterin was injected into rats intravenously in the form of albumin-stabilized emulsion. In 2--4 h and then every day 3H2O radioactivity of one of the cholesterin enzymatic hydroxylation products in microsomal liver apparatus was estimated in animals' urine.

[Prevention of atherogenic dislipoproteinemias and metabolic disorders in the liver in emotional-pain stress].

Atherogenous dislipoproteinemia, involving a decrease in HDL cholesterol and 3-4-fold increase in the atherogeneity index was found to develop in rats after emotional-pain-dependent stress. Lipid peroxidation was activated in liver tissue of the animals, which was expressed as an increase in the MDA content, a decrease in SOD activity and as marked activation of fructose I-phosphate aldolase, an enzyme specific for liver tissue, in blood serum. The impairment of liver tissue caused an inhibition of 7 alpha-cholesterol hydroxylase--key enzyme of cholesterol hydroxylation into bile acids; the phenomenon may be of importance in development of dislipoproteinemias.

[Effect of adaptation to hypoxia on the antioxidant enzyme activity in the liver in animals that have undergone stress].

It was shown in experiments on rats that emotional-painful stress resulted in a rapid increase in malonic dialdehyde (MDA) and in a decrease in the activity of superoxide dismutase (SOD) in liver. Adaptation to moderate intermittent hypoxia in altitude chamber did not affect MDA and increased hepatic SOD by 65%. Stress exposure caused no change in SOD and MDA, but abruptly reduced the fall of SOD in adapted animals.

[Effect of emotional and pain stress on the level of antioxidant vitamins in the blood serum of rats].

The content of ascorbic acid and alpha-tocopherol was found to be decreased in the blood of rats which had suffered an emotional pain stress. Preadaptation of the animals to hypoxia did not change the level of ascorbic acid, but it was valuable with respect to alpha-tocopherol. The emotional pain stress in the presence of adaptation to hypoxia induced in the animals reduction of the blood levels of both vitamins similar to that in the controls.

[Prevention of stress dyslipidemia by adapting animals to the periodic action of hypoxia].

Emotional-painful stress in rats results in the increase of atherogenic and decrease of antiatherogenic lipoprotein fractions. Adaptation of animals to periodic intermittent hypoxia significantly enhanced the proportion of antiatherogenic lipoproteins in the blood and reduced the degree of post-stress dyslipidemia.

[Role of lipid peroxidation in inhibiting cardiac Na, K-ATPase during stress].

Induction of lipid peroxidation (LPO) under emotional painful stress in rats in vivo and by the Fe2+ plus ascorbate system in vitro results in inactivation of Na,K-ATPase in the sarcolemma-rich membrane fraction of the heart. Activity of Mg-ATPase remains practically unchanged. The scavenger of lipid free radicals 4-methyl-2,6-ditertbutylphenol (ionol) prevents Na,K-ATPase inactivation in both cases.

[Activity of Krebs cycle dehydrogenase and tissue respiration enzymes in cerebral hemispheres of rats under stress].

It is established that emotional-painful stress and myocardium necrosis evoked in animals after the emotional-painful stress is accompanied by a disturbance in the creative metabolism and partial inhibition of cytochrome oxidase in cerebral hemispheres. A conclusion is made that the found changes may be one of the pathogenetic factors in formation of the neurosis-like states under stress and diseases originated from the effect of the emotional-psychic overstrain.