[Bone marrow as an organ of erythrocyte destruction in hematological disorders].

Bone marrow of patients with hematological diseases contains a great number of erythroclasic clusters characterized by exocytic lysis of the constituent erythrocytes by cluster-forming myelocaryocytes including erythrocaryocytes. The content of erythroclasic clusters with exocytic lysis of erythrocytes varied from 21% of total erythroclasic clusters in bone marrow of patients with aplastic anemia to 81% in bone marrow of patients with an active phase of acute lymphoblastic leukemia showing high intensity of hemolysis in the bone marrow. Most intensive lysis of erythrocytes in erythroclasic clusters took place in the bone marrow of patients in an active stage of acute lymphoblastic leukemia and patients with chronic myeloid leukemia. At the time of the investigation tens of thousands of erythrocytes were undergoing destruction in erythroclasic clusters in one mcl of bone marrow of such patients. These findings confirm the idea of the bone marrow as an organ of erythrocyte destruction.

[Changes in lipid contents of the myocardium in rats during physical loading after long-term hypokinetic stress]. / Izmenenie lipidnogo sostava miokarda u krys pri fizicheskikh nagruzkakh posle vozdeistviia dlitel'nogo gipokineticheskogo stressa.

During prolonged motor restraint rearrangement of the lipid bilayer of membranes in the aortic ventricle of the heart progresses in parallel to atrophy of its contractile system. This rearrangement is characterised by a decrease in cholesterol and an increase in relative content of unsaturated phospholipids, initially contributing to activation of the lipid-dependent enzymatic systems, and more effective electromechanical conjugation. However, subsequent accumulation of toxic products of lipids peroxidation indicative of disturbed adaptation mechanisms involved in stress-reaction resulted in damage to the myocardial membranes, variations in the bioelectrical properties and deteriorated contractility, and diastolic relaxation of the cardiac muscle. Consequently, heart adaptability to load was reduced in the period of readaptation after hypokinesia. On the background of energy deficiency with subdued synthesis of contractile muscle proteins, levels of cholesterol, triglycerides and especially free fatty acids went up. Along with lipid peroxides these agents disrupt functioning of subcellular organelles and limit adaptation potentials of deconditioned heart.

[The anti-arrhythmic action of exogenous creatine phosphate and its effect on myocardial electrophysiological parameters in acute heart failure]. / Antiaritmicheskoe deistvie ékzogennogo kreatinfosfata i ego vliianiia na élektrofiziologicheskie parametry miokarda pri ostroi serdechnoi nedostatochnosti.

The experiments on rats with overload heart failure have shown that creatine phosphate (CP) used in a single dose at the peak of severe signs of cardiac decompensation was found to produce a short-term normalization of rhythm and an increase in heart rate. With multiple doses, the agent slowed down the development of bradycardia, prevented arrhythmias and promoted the rise of longevity in the experimental animals. At the same time, exogenous CP failed to affect energy-dependent processes of re- and depolarization which were impaired in the myocardium in acute heart failure.

[Mechanism of self-maintenance of experimental atherogenic hyperlipoproteinemia]. / O mekhanizme samopodderzhaniia éksperimental'noi aterogennoi giperlipoproteinemii.

Disorders of lipid catabolism in the liver and increased formation and intensified secretion into the blood of lipoproteins synthesized in the liver evidently play a significant role in the maintenance of experimental atherogenic hyperlipoproteinemia induced in rabbits by prolonged administration of atherogenic lipoproteins.

[Effect of exogenous creatine phosphate on electrophysiologic myocardial parameters in overload heart failure]. / Vliianie ékzogennogo kreatinfosfata na élektrofiziologicheskie parametry miokarda pri peregruzochnoi forme serdechnoi nedostatochnosti.

Experiments with rats undergoing overload testing showed that exogenous creatine phosphate was likely to fail to penetrate into myocardiocytes and to affect their energy balance directly. However, during its long-term administration in energy deficiency, creatine phosphate was able to maintain cardiac pump function via activation of processes controlling sinus nodal automatism and atrioventricular conduction.

[Changes in lipid metabolism in the myocardium as one of the possible mechanisms of the development of the overload form of heart failure]. / Izmenenie obmena lipidov v miokarde kak odin iz vozmozhnykh mekhanizmov razvitiia peregruzochnoi formy serdechnoi nedostatochnosti.

In addition to hypertrophy of the myocardium, there are changes in its lipid composition as evidenced by activated lipid peroxidation, lower quantities of unsaturated fatty acids, and higher amounts of saturated phospholipids and lysophospholipids in overload heart failure induced by aortic coarctation. The derangement of the lipid environment may contribute to a decrease in the powerful capacity of membraneous enzyme systems, disturbances in ion transport and cardiac diastolic relaxation, which is one of the causes of heart failure.

[Change in myocardial phospholipid composition in cardiac hyperfunction as one of the possible prerequisites of sudden death]. / Izmenenie fosfolipidnogo sostava miokarda pri giperfuktsii serdtsa kak odna iz vozmozhnykh metabolicheskikh predposyok vnezapnoi smerti.

It is shown that additional load on a compensatory hypertrophied heart disturbs its adaptation mechanisms. Lipid peroxidation is activated, the amount of some types of unsaturated phospholipids reduces, and lysophospholipids, detergents damaging the cell membranes and causing an arrhythmogenic effect accumulate.

[The lipid and phospholipid composition of the myocardium in hyperfunction caused by aortic coarctation]. / Lipidnyi i fosfolipidnyi sostav miokarda pri ego giperfunktsii, vyzvannoi koarktatsiei aorty.

It is shown that in the first 10-12 days of heart hyperfunction caused by subdiaphragmatic constriction of the aorta adaptational changes in lipid metabolism develop in the myocardium in addition to its hypertrophy. These changes are capable of leading to reduced viscosity of the myocardial membranes and activation of enzymatic processes providing for the intensified work of the heart.

[The metabolic changes in myocardial subcellular fractions in the pathogenesis of ischemic heart disease]. / Metabolicheskie izmeneniia subkletochnykh fraktsii miokarda v patogeneze ishemicheskoi bolezni serdtsa.

In the myocardial mitochondria (MCh) of persons who had died from ischemic heart disease (IHD) the content of phosphatidylcholine (PCh) and cardiolipin reduces while the amount of the products of their hydrolysis--free fatty acids (FFA) and lysophospholipids--increases. This is evidence of the breakdown of the membrane MCh phospholipids (PL). The content of PL, protein, FChS, FFA, and lysophosphatidylethanolamine in the sarcoplasmic reticulum increases. The increase in the amount of PL, protein, and free cholesterol (FChS) may be explained by an increase of their synthesis due to myocardial hypertrophy which was encountered in all of the cases studied. The accumulation of FFA and lysophosphatidylethanolamine is probably not linked with PL hydrolysis (their amount in this subcellular fraction increases) but is a consequence of other changes in myocardial lipid metabolism. Thus, in IHD hydrolysis of PL prevails in the myocardial MCh and their synthesis in the sarcoplasma reticulum. These changes in the metabolism of the subcellular fractions may lead to damage of the membranes of the cardiomyocyte MCh, which may be the cause of disorders of electrolyte metabolism and contractile properties of the myocardium in IHD.

[Pathogenesis of alcohol-induced disorders of lipid metabolism in the myocardium]. / Patogenez vyzvannykh alkogolem narushenii lipidnogo obmena miokarda.

It was found that in the myocardium of the individuals who had died from acute alcoholic intoxication and the animals given ethanol the content of anaerobic M-isoforms of lactate dehydrogenase increased that indicated the activation of anaerobic glycolysis.

[Lipid and phospholipid composition of the rat myocardium during adaptation to physical exertion]. / Lipidnyi i fosfolipidnyi sostav miokarda krys pri adaptatsii k fizicheskoi nagruzke.

Adaptation to progressively increasing physical stress causes cardiomyocyte hypertrophy as well as increased levels of unsaturated phospholipids and cholesterol esters and a simultaneous relative depression of free cholesterol synthesis and lipid peroxidation in the rat myocardium.

[The effect of hyperlipoproteinemia induced by the administration of an atherogenic lipoprotein fraction on various indices of lipid metabolism in rabbits]. / O vliianii giperlipoproteidemii, indutsirovannoi vvedeniem aterogennoi fraktsii lipoproteidov, na nekotorye pokazateli lipidnogo obmena u krolikov.

Hyperlipoproteinemia, which was developed after intravenous administration of lipoprotein atherogenous fraction, caused the secondary metabolic alterations. These alterations were manifested as a decrease in catabolism of blood serum lipoproteins, accumulation of hydrophobic lipid components in the lipoproteins as well as in a decrease in relative content of high density lipoproteins responsible for elimination of cholesterol from tissues.

[Mechanism of the maintenance of experimental hyperlipoproteinemia in the rabbit]. / O nekotorykh mekhanizmakh podderzhaniia éksperimental'noi giperlipoproteidemii u krolikov.

A decrease in lipolytic and total esterase activities as well as an increase in the rate of cholesterol esterification were found in blood of rabbits with experimental hyperlipoproteinemia caused by intravenous administration of atherogenic lipoproteins. Simultaneously, content of free and esterified cholesterol was increased in liver tissue, content of triglycerides and phospholipids was decreased in mitochondria; the lipolytic activity was elevated.

[Glucose-6-phosphate dehydrogenase and lactate dehydrogenase activities and lactate dehydrogenase isoenzyme spectrum in human myocardium after sudden death caused by acute alcohol intoxication and ischemic heart disease]. / Aktivnost' gliukozo-6-fosfatdegidrogenazy i laktatdegidrogenazy i izofermentnyi spektr laktatdegidrogenazy v miokarde lits, umershikh vnezapno ot ostrogo otravleniia étanolom i ot ishemicheskoi bolezni serdtsa.

Alterations in activities of lactate- and glucose-6-phosphate dehydrogenases and in the LDHisozyme spectra in human heart muscle after sudden death, caused either by acute ethanol intoxication or by ischemic heart disease, were characterized by inhibition of aerobic oxidation and activation of the glycolytic pathway of energy formation.