[The anticytolytic activity of ubiquinone-10 in a liver lesion from chlorinated hydrocarbons]. / Antitsitoliticheskaia aktivnost' ubikhinona-10 pri porazhenii pecheni khlorirovannymi uglevodorodami.

Antioxidative activity of ubiquinone-10, exceeding the level of that of vitamin E more than five times and anticytolytic activity of vitamin E and particularly of ubiquinone-10 manifested in decreasing activities of blood serum alanine aminotransferase and histidineammoniumlyase, which might be determined only during toxic liver damage, have been demonstrated. The activity of histidineammoniumlyase was considerably decreased under the effect of vitamin E and particularly in the presence of ubiquinone-10. Decreasing of activity of blood serum enzyme markers of cytolysis of hepatocytes is connected with the hepatocytes biomembrane stabilizing effect of antioxidants which was confirmed by the electron microscope investigation method. The evidence of safety of intact cellular and subcellular membranes and activation of compensative and regenerative processes in hepatocytes was also represented.

[Morphological changes in the liver in primary sclerosing cholangitis (a histological and electron microscopic study)]. / Morfologicheskie izmeneniia pechni pri pervichnom skleroziruiushchem kholangite (gistologicheskoe i élektronno-mikroskopicheskoe issledovanie).

9 cases (males) of primary sclerosing cholangitis (PSC) were studied clinico-morphologically. In puncture liver biopsies, sclerosis of walls of big ducts and portal tracts was found in 2 cases only; cell infiltration was minimal. Lobular hepatitis with intralobular fibrosis and moderate sclerosis of portal stroma was found in 3 patients, monolobular inactive liver cirrhosis in 4 patients. In all cases mild intralobular cholestasis was found which was followed with a considerable increase of copper and manganese in the liver and serum. The accumulation of a large amount of collagen of different types was observed around bile ducts which ultrastructurally was seen as fibrillar structures and homogeneous substance similar to the basal membrane. The elements of the epithelium destruction were found in foci of the duct basal membrane alteration, in the absence of cell infiltration. Progressing fibrosis of both portal tracts without inflammation and individual segments of the bile ducts and the intralobular stroma is at the basis of PSC.

[Role of sinusoidal cells in the morphogenesis of alcoholic liver cirrhosis]. / Rol' sinusoidal'nykh kletok v morfogeneze alkogol'nogo tsirroza pecheni.

49 liver biopsies in alcoholic liver damage (fibrosis, chronic persisting hepatitis, cirrhosis) are studied on semithin sections electron microscopically and morphometrically. Morphological varieties of hepatocytes and sinusoidal cells are revealed as well as some rules in their proportions. Domination of stellate reticulo-endotheliocytes with a high secretory and phagocyte activity correlates with high adaptive properties of hepatocytes and transformation of lipocytes into fibroblast-like cells without development of intralobular fibrosis. If nonactive variant of the stellate reticulo-endotheliocytes prevails, the number of damaged hepatocytes and fibroblast-like lipocytes increases, intralobular fibrosis becomes pronounced resulting in hepatocyte death. Role of sinusoidal cells in realization of alcoholic cirrhosis morphogenesis is discussed.

[The morphological characteristics of hepatocyte dysplasia]. / Morfologicheskaia kharakteristika displazii gepatotsitov.

27 liver biopsies of patients with chronic hepatitis and liver cirrhosis of viral etiology were studied histologically, electron microscopically and morphometrically. Hepatocyte dysplasia is characterized by the disturbance of the liver lobule structure and alteration of the liver tissue regeneration. Dysplasia is manifested light microscopically by the three types of cells: large, "average" and small ones. Electron microscopically (EM) 4 varieties of dysplastic hepatocytes can be distinguished: (1) with developed cytoplasmic network, (2) with hyperplasia of mitochondria, (3) with underdeveloped organelles, (4) with highly atypical nuclei. There exists a correlation between the light microscopic and EM types of dysplasia: the 1st and the 2nd types are typical for the "average" cell dysplasia, the 3rd for the large cell and the 4th for the small cell dysplasia. The latter two ultrastructural varieties can be considered as manifestations of severe dysplasia. One of them is characterized by the large size of cells, the presence of two or three nuclei, nucleus-cytoplasmic ratio 0.3-0.4 and pronounced signs of atypical ultrastructural organization in the form of the underdevelopment and deformity of the cytoplasmic network and mitochondria. Another variety of dysplastic hepatocytes is represented by small basophilic cells with hyperchromic deformed nuclei, high nucleus-cytoplasmic ratio (greater than 0.4) and the signs of lowering the differentiation/underdevelopment of the granular cytoplasmic network, ribosome hyperplasia, the absence of the mature intercellular contacts.

[Experimental antioxidant therapy in toxic liver damage from CCl4 and chloxyl]. / Eksperimental'naia terapiia antioksidantami pri toksicheskom povrezhdenii pecheni CCl4 i khloksilom.

The authors studied the pharmacotherapeutic efficacy of antioxidants vitamin E, sodium selenite, and their combination in damage to rat liver by CCl4 and the anthelmintic agent chloxyl. Changes of the intensity of peroxidation of biological membrane lipids, the activity of enzymes-markers of hepatocyte cytolysis--alanine aminotransferase and aspartate aminotransferase--in blood serum, and changes in the structure of the liver were studied. Antioxidants and their combination blocked lipid peroxidation, reduced the activity of alanine aminotransferase and aspartate aminotransferase in blood serum considerably, and caused a protective effect on the structure of rat liver in its damage by CCl4 and chloxyl.

[Pathogenetic mechanisms of liver damage by the anthelmintic preparation chloxyl]. / O patogeneticheskikh mekhanizmakh porazheniia pecheni antigel'mintnym preparatom khloksilom.

The pathogenetic mechanisms of hepatotoxicity of an anthelminthic drug chloxyl as compared with the mechanisms of CCl4 hepatotoxicity were studied on the basis of the change of the liver content of the primary (conjugated dienes) and secondary (malondialdehyde) products of lipid peroxidation. the activity of alanine aminotransferase and aspartate aminotransferase in the blood serum of rats and on the basis of the change of the liver structure. The pathogenetic mechanisms of chloxyl hepatotoxicity are close to those of CCl4 and consist in the activation of membrane lipid peroxidation, that is, an increase of the liver contents of the primary and secondary products of lipid peroxidation, an impairment of permeability of membranes of hepatocytes and their destruction with the release in the blood of cytoplasmic enzymes of alanine aminotransferase and aspartate aminotransferase.

[Morphological bases of liver insufficiency in the early stages of the prolonged crush syndrome]. / Morfologicheskie osnovy pechenochnoi nedostatochnosti v rannem periode sindroma dlitel'nogo razdavlivaniia.

Light and electron microscopies were employed to examine liver of 45 rats and 20 dogs under 6- and 9-hour compression of soft tissues of the thigh and 2 to 7 hours after pressure was taken off. Morphology of liver microcirculatory disorders is presented, the incremental derangement of the cells of the reticuloendothelial system (RES) with the appearance of the signs of its function depletion after decompression is described. Alterations in the liver RES correlated with destructive changes in hepatocytes and their necrosis. The morphological alterations in the liver RES in the crush syndrome reflect the impairment of its barrier function. They may play a role in the impairment of liver regeneration processes and immunological homeostasis of the host.

[Morphology of the liver in experimental shock]. / Morfologiia pecheni pri éksperimental'nom shoke.

The authors' and literature data on the liver changes at different types of shock are summarized with consideration of the role of etiology and pathogenetic factors. Three groups of similar liver alterations reflecting the severity of impairment of the reticulo-endothelial system (RES), microcirculation and parenchyma are distinguished. No clear-cut dependence between the liver morphological changes and the severity of shock is noted. At the same time the characteristic structural alterations for some forms of shock differing at their early stages by a predominance of neuro-reflectoral, hypovolemic or toxic component are revealed. A rapidly developing hydropic degeneration, the absence of the compensatory changes, signs of the RES deficiency with the progressing necrobiotic and necrotic processes in the liver are characteristic for a neuro-reflectoral shock. Endotoxic shock is associated with widespread intravascular thrombi, liver cell necrosis, combination of the destruction of reticuloendotheliocytes with the signs of their preceding activation, foci of a smooth cytoplasmic network hyperplasia of centrolobular hepatocytes; hypovolemic shock is characterized by activation of compensatory processes.

[Granulomatous hepatitis]. / Granulematoznyi gepatit.

The diagnosis of granulomatous hepatitis was made on the basis of granulomas observed in the liver biopsies from 64 patients. It is shown that the macrophagal granulomas are, as a rule, localized inside the lobules, do not possess the characteristic features and represent the morphological manifestations of a non-specific reactive hepatitis. At the same time macrophagal granulomas may be a stage in the formation of the epithelioid-cell granulomas. The latter reflect the long persistence of the antigen in the liver macrophages. In certain cases the epithelioid-cell granulomas acquire specific features and these allow one, when analysing the liver biopsies, to confirm or to suggest the etiology of the disease (sarcoidosis, tuberculosis). An essential help in establishing the etiology of granulomatous hepatitis comes from the repeated clinical examination of patients and repeated liver punctures.

[Morphologic characteristics of disorders of liver function in myasthenia]. / Morfologicheskaia kharakteristika narushenii funktsii pecheni pri miastenii.

Clinico-morphological study of the liver was carried out in 54 patients with generalized severe myasthenia of 1 1/2-2-year duration. The functional values of the liver were studied before thymectomy and on the 1st post-operation day. Eight liver punctates were examined histologically and electron-microscopically. A picture of nonspecific reactive hepatitis whose clinical manifestations included hyperbilirubinemia, and disorder of the absorbing and excreting functions of the liver was revealed. Ultrastructural signs of cholestasis were found. The observed fibrosis of the organ was accompanied by hypertrophy and hyperplasia of lipocytes but without their manifest transformation into lipofibroblasts . Hypoplasia of hepatocytes was observed in myasthenia which may be due to their thymus-dependent inhibition. The mechanism of disturbance of pigment metabolism in the liver of patients with myasthenia is multi-component and may be associated with disorders in bile evacuation, hematotissue barrier, and probably, structural-functional incompetence of hepatocytes.

[Morphological diagnostic criteria of nonspecific reactive hepatitis]. / Kriterii morfologicheskoi diagnostiki nespetsificheskogo reaktivnogo gepatita.

The material of 100 punch liver biopsies from patients with a secondary nonspecific reactive hepatitis as a complication of chronic disease of the alimentary canal (gall bladder, pancreas, stomach and intestine) was studied. The criteria of morphological diagnostics of this hepatitis were elaborated. It is established that the morphology of the nonspecific reactive hepatitis depends on the pathogenesis and clinical course of the underlying disease. The response of liver macrophagal system is a basis of inflammatory changes.

[Clinico-morphological characteristics of liver diseases associated with nonconjugated hyperbilirubinemia syndrome]. / Kliniko-morfologicheskaia kharakteristika zabolevanii pecheni, protekaiushchikh s sindromom nekon'iugirovannoi giperbilirubinemii.

Altogether 98 puncture liver biopsies taken from patients with a syndrome of nonconjugated hyperbilirubinemia are examined in light and electron microscope. It is established that this syndrome frequently develops in inflammatory liver diseases, notably in primary (viral, alcoholic, medicinal) and secondary (nonspecific reactive) hepatitis. Both light and electron-microscopic investigation of liver puncture biopsies allows determining the type of a pathological process in the liver, to specify its etiology and to study the structural basis of bilirubin metabolic disorders in the liver. The mechanism of these metabolic disorders is complex and includes alteration of the bilirubin seizure by a sinusoidal hepatocyte pole, its conjugation and formation of ultimate metabolites.

[Sinusoidal cells of the liver and their role in pathologic processes]. / Sinusoidal'nye kletki pecheni i ikh rol'v patologicheskikh protsessakh.

The review summarizes the data on morphofunctional properties and histogenesis of 4 types of sinusoidal cells of the liver: stellate reticuloendotheliocyte (SR), endotheliocyte, lipocyte and Pit-cells. It is suggested that they be considered as a single structural-functional system forming the hematotissue barrier, the connective tissue skeleton of the lobule and taking part in neurohumoral regulations of the local processes. Most attention is given to SR which are the main element of the hepatic reticuloendothelial system. The participation of SR in the pathogenesis of hepatitis, cirrhosis of the liver, and some extrahepatic diseases has been shown to be connected not only with the disturbance of their phagocytic function but also with the deficiency in formation and correction of local immune reactions as well as the entire immune system. It is assumed that uncompensated insufficiency of the hepatic reticuloendothelial system may facilitate chronization of the pathological process in the liver as well as the development of some of its complications.

[Ultrastructural bases of heart failure in the early period of the prolonged crush syndrome]. / Ul'trastrukturnye osnovy serdechnoi nedostatochnosti v rannem periode sindroma dlitel'nogo razdavlivaniia.

Histological, electron microscopic, and physiological studies on the myocardium of rats and dogs in severe forms of compression syndrome (6-9 hours of compression and 2-4-7 hours after decompression) revealed three groups of morphological changes underlying cardiac insufficiency: (1) predominantly microcirculatory disorders with mild changes in cardiomyocytes detectable in bradycardia. Under these conditions the development of cardiac weakness may be based on both calcium overloading and reflectory weakening of the heart activity; (2) combination of microcirculatory disorders with marked hypoxic damage of the cardiomyocytes structure detectable under conditions of tachycardia may be an independent cause of the cardiac muscle weakness; (3) changes in the structures of cardiomyocytes responsible for nervous impulses conduction: sarcolemma and its derivatives. Under this condition, the probable cause of cardiac disorders may be electrolyte imbalance accompanying postcompression toxemia.