Search PubMed⌕ Search

Biomedical subjects

O P Molodykh

Publications and source records attributed to O P Molodykh.

16 recordsLinked to original sources
PubMed2006

Structural reorganization of the rat liver under cytotoxic effect of doxorubicin.

We studied structural reorganization of the liver after toxic injury caused by a single injection of doxorubicin in a sublethal dose (10 mg/kg). The morphogenesis of doxorubicin injury to the liver is determined by two main pathogenetic factors: cytotoxic effect of doxorubicin and its metabolites on liver cell populations (primarily hepatocytes) and pronounced hemodynamic disorders in the greater circulation resulting from the development of chronic cardiac insufficiency. Changes in hepatocyte caused by doxorubicin manifest by fatty degeneration in the periportal zones and by pronounced lytic changes in the pericentral zones, most pronounced by day 30 of the experiment. Doxorubicin in the studied dose exhibited no cytostatic effect on the hepatocyte population. Hepatocyte proliferation, observed during the entire experiment, leads to an appreciable increase in their count and liver weight.

Animals↗
PubMed2005

Ultrastructural criteria of cardiomyocyte regeneratory and plastic insufficiency in anthracycline cardiomyopathy.

We analyzed the dynamics of ultrastructural changes in cardiomyocytes in experimental chronic anthracycline cardiomyopathy. Doxorubicin-induced changes in cardiomyocytes were characterized by a specific combination of ultrastructural changes, which can be regarded as markers of the development of regeneratory and plastic insufficiency. These markers include a triad of changes: deformation of the nuclei with reorganization of the nucleolar system; diffuse and small focal lysis of myofibrils (mainly fine filaments); dilatation of agranular sarcoplasmic reticulum and the intermembrane perinuclear space connected to it. The terminal stages of these disorders are degeneration of some cardiomyocytes, their apoptotic death, and resorption by mononuclear cells (processes representing successive stages in the development of regeneratory and plastic insufficiency of the myocardium).

Animals↗
PubMed2005

Tissue and intracellular reorganization of rat liver during total body hypothermia.

We studied tissue and intracellular reorganization of the liver during total body hypothermia and evaluated regeneration strategies at different levels of structural organization. Hypothermia results in morphofunctional changes in the liver (degeneration, lysis, necrobiosis, and focal necrosis of hepatocytes developing against the background of disorders in blood and lymph circulation). Decreased sinusoid/hepatocyte volume ratio is the key factor in tissue reorganization of the liver. Intracellular reorganization of hepatocytes is characterized by dysproportional changes in the volume and surface densities of the main cytoplasmic organelles involved in biosynthesis and energy production.

Animals↗
PubMed2005

[Ultrastructural manifestations of disturbances of cardiomyocyte regeneration after the doxorubicin treatment].

The pattern of cardiomyocyte intracellular reorganization following administration of a antibiotic of anthracyclin series, doxorubicin, was studied. Cardiomyocyte injury following doxorubicin treatment included a triad of ultrastructural changes: nuclear deformation with a reorganization of nucleolar apparatus; diffuse and fine focal lysis of myofibrils, and a dilation of agranular sarcoplasmic reticulum with an associated perinuclear space. As the terminal stages of such disturbances, atrophy of some part of cardiomyocytes, their apoptotoc death and a resorption by mononuclear cells were found, which are the processes demonstrating successive stages of development of regenerative-plastic myocardial insufficiency and resulting in a dilation remodeling of the heart.

Animals↗
PubMed2004

Morphological manifestations of heart remodeling in anthracycline-induced dilated cardiomyopathy.

The morphogenesis of anthracycline-induced dilated cardiomyopathy was studied after single sublethal dose of doxorubicin. Cardiomyocyte depopulation (up to 27%) and decrease in their regeneratory plastic reactions were the main mechanisms of cardiac failure development after anthracycline (doxorubicin) treatment, determining the type of heart remodeling by the dilatation variant. Cardiomyocyte elimination and atrophy during the development of anthracycline-induced regeneratory plastic cardiac insufficiency were paralleled by hypertrophy of remaining cardiomyocytes and diffuse and small focal sclerosis of the myocardium, which could be regarded as a correlated compensatory reaction of the connective tissue to the decrease in the number of muscle fibers.

Animals↗
PubMed2000

Death, elimination, and regeneration of cardiomyocytes in mice after hyperthermia.

Single total hyperthermia changed the absolute number of cardiomyocytes in experimental animals. The total number of cardiomyocytes decreased by 20% (without signs of their necrosis) on day 3 of post-heating restitution and then returned to the control. This was probably related to cytokinesis (without karyokinesis) of binucleated cells, whose content considerably decreased during recovery.

Animals↗
PubMed2000

Apoptosis: decrease of hepatocyte population in mice after hyperthermia.

hyperthermia caused hemodynamic disorders in the liver and degenerative and necrobiotic changes in hepatocytes of CBA mice. Total hepatocyte count decreased during restitution, this decrease being most pronounced 30 min after exposure. The number of binucleated cells also markedly decreased. The absence of necrotic changes in hepatocytes during the entire restitution period indicated their apoptotic death and elimination by macrophagal resorption. Under these conditions liver regeneration at the cellular level occured mainly via division of binucleated hepatocytes. On the other hand, proliferation of oval cells in the portal zones and their differentiation into hepatocytes were observed at certain stages of reparative regeneration of the liver.

Animals↗
PubMed1993

[A quantitative tissue analysis of the rat myocardium in whole-body overheating].

The reorganization of Wistar rat myocardium at 3 and 7 days after a single total overheating at a temperature of 43 degrees C was studied using stereologic and qualitative morphological tissue analysis. Most pronounced morphofunctional changes in myocardium were shown to develop 3 days after the exposure such as hemodynamic disorders, lymphostasis, interstitial edema, contracture lesions of cardiomyocytes. The spatial myocardial reorganization was not considerable. At 7 day after exposure, a significant decrease of the heart weight as a result of atrophic changes in cardiomyocytes was recorded. In the same period the most pronounced spatial reorganization of myocardial parenchyma and stroma was noted. The significant decrease of volume density of capillaries was accompanied by some increase of the volume density of cardiomyocytes resulting in a significant decrease of volume ratio of capillaries to cardiomyocytes. Thus, during postheating restitution the atrophy of myocardium developed characterized by an unbalanced decrease of volume densities of capillaries and cardiomyocytes.

Animals↗
PubMedDate not supplied

[Morphological study of the liver of mice-like rodents from areas of the Altai region exposed to radioactive pollution].

Morphofunctional liver state of two mice-like rodents species caught at the three areas of Altai region exposed to radiation during nuclear tests at Semipalatinsk site was studied. It was shown that the stereotype morphofunctional changes in the liver of both rodent species were developed under chronic influence of low doses of radiation and chemical contamination. These changes are manifested as dystrophic disorders of hepatocytes and hemodynamic disturbances accompanied by a decrease of volume ratio of sinusoidal capillaries to hepatocytes and stroma to parenchyma. Hyperglycogenosis, redistribution of the main cytoplasmic organelles, and considerably reduction of the volume densities of mitochondria, smooth and rough endoplasmic reticulum are the leading ultrastructural changes. Moreover, character and manifestation of the changes are determined by ecological belonging and correlated with intensity of anthropogenic pollution. The role of these changes in development of long-term pathology are discussed.

Animals↗