Biomedical subjects

L M Nepomnyashchikh

Publications and source records attributed to L M Nepomnyashchikh.

At least 19 recordsLinked to original sources

PubMed2003

Morphological and stereological characteristics of myocardial remodeling in aged spontaneously hypertensive SHR rats.

Myocardial remodeling in SHR rats with age-related hypertrophy was characterized by elimination of cardiomyocytes, their hypertrophy, and marked increase in the volume of the connective tissue. The count of cardiomyocytes with contracture injuries and subsegmental contractures increased, and pronounced perivascular and interstitial sclerosis developed in the hypertrophic myocardium of SHR rats. Damage to the microcirculatory bed manifested in degenerative changes and destruction of some endotheliocytes. Signs of atypical intracellular regeneration in myofibrils and impairment of their longitudinal orientation were revealed in cardiomyocytes in the late stage of compensatory hypertrophy.

Aging↗

PubMed2003

Pathomorphology of the vascular bed of postinfarction heart in various types of remodeling.

We evaluated pathomorphological changes in the vascular bed of postinfarction heart in various types of remodeling. Dilatational remodeling was characterized by dilation of coronary arteries, increase in their volume density, and regular arrangement. Signs of coronary blood flow reduction and microcirculatory disturbances in the left ventricle were revealed during hypertrophic remodeling. Aneurysmal remodeling was characterized by the presence of small-vascular collateral-anastomotic plexus and reduction of the microcirculatory bed. Endocardial remodeling was accompanied by hypervascularization of the myocardium, formation of new coronary vessels, and reduced capillarization in the left ventricle of postinfarction heart.

Coronary Angiography↗

PubMed2002

Parenchyma-stroma relationships in the myocardium: alterative insufficiency of cardiomyocytes and morphogenesis of focal cardiosclerosis.

Remodeling of the myocardium during focal metabolic damages to cardiomyocytes is determined by contracture injuries to myofibrils, their lump degradation, and development of coagulation necrosis. Reactive changes in the stroma develop over the first hours and manifest in acute hemodynamic disturbances followed by proliferation of connective tissue cells. The immature granulation tissue is formed at the site of myocardial damages. Later this tissue is replaced by the mature connective tissue with the formation of small scars. It should be emphasized that sclerotic changes during remodeling of the myocardium after focal metabolic damages are reversible.

Animals↗

PubMed2002

Biosynthetic reactions and ultrastructure of urothelial cells in chronic cystitis and cystopathies.

A new form of morphogenesis of pathological process, cystopathy, was distinguished on the basis endoscopy data and morphofunctional analysis of the urinary bladder in chronic cystitis. Cystopathy is characterized by predominance of diffuse degeneration and atrophy of the urothelium, stromal sclerosis, absence of inflammatory cell infiltration, and inhibition of biosynthetic reactions in urothelial cells (compared to chronic cystitis). Cystopathy results from regeneratory and plastic failure. Instability of the bladder epithelium can be a morphological marker of oncological risk.

Adolescent↗

PubMed2002

Allergic dermatoses associated with chronic opisthorchiasis during antihelminthic therapy.

We studied skin biopsy specimens from patients with allergic dermatoses associated with opisthorchiasis. Structural changes in the epidermis and derma were presented by degenerative and destructive changes in epitheliocytes with a pronounced membranolytic component, hemodynamic disturbances in the derma, disorganization of the connective tissue, and progressive fibrosis. Combination therapy including antihelmintic drug produced a positive effect, which was associated with induction of regenerative processes in basal epidermal cells, stabilization of the basal membrane, and normalization of the dermoepidermal junction. Our findings indicate that opisthorchiasis plays an important role in the pathogenesis of allergic dermatoses.

Anthelmintics↗

PubMed2002

Lytic and contracture-lytic prenecrotic damage to cardiomyocytes: photochemical fluorochrome staining and fluorescent microscopy of the myocardium.

Acute prenecrotic damage to cardiomyocytes of lytic (myocytolysis, cytolysis) and contracture-lytic (primary lumpy degradation of myofibrils) types during ischemic and metabolic alteration of the myocardium are detected at the photooptic level by means of photochemical fluorochrome staining and examination under fluorescent light. Comparison of the fluorescent and polarization microscopic pictures showed that changes in cardiomyocytes are determined by local mass redistribution in the sarcomere compartments and transformations of birefraction of myofibrillar system components during necrobiosis. These changes are determined by lysis and coagulation processes in protein structures of sarcomeres.

Animals↗

PubMed2002

Pathomorphology of myocardial bridges and their role in the pathogenesis of coronary disease.

The hearts of patients who died of coronary disease and had myocardial bridges were studied by postmortem coronary angiography, cardioventriculography, and complex pathomorphological analysis. The relationship between the incidence and pathomorphology of myocardial bridges, on the one hand, and the type of blood supply, segmentary topography of the major coronary arteries, geometry of the left ventricle, and coronary changes in different forms of coronary disease, on the other, was analyzed. Diagnostic criteria were developed and the main components of the etiology, patho- and thanatogenesis in coronary patients with coronary arteries not affected by atherosclerosis are presented.

Adult↗

PubMed2001

Alterative and plastic insufficiency of cardiomyocytes: isoproterenol-induced damage to myocardium during anthracycline cardiomyopathy.

The development of regenerative and plastic myocardial insufficiency induced by anthracycline antibiotic rubomycin is accompanied by a decrease in cardiomyocyte sensitivity to damage produced by synthetic catecholamine isoproterenol. The incidence and the size of coagulation necrosis foci of cardiomyocytes developed 6 h after isoproterenol injection significantly decreased with increasing in the interval between rubomycin injection and subsequent administration of isoproterenol. In Wistar rats receiving rubomycin 3-5 days prior to isoproterenol and exhibiting signs of regenerative and plastic insufficiency, no cardiomyocyte contracture, intracellular myocytolysis, or lump degradation characteristic of cardiac insufficiency induced by endo- and exogenous catecholamines were found.

Animals↗

PubMed2001

Relationships between myocardial parenchyma and stroma: regenerative and plastic insufficiency of cardiomyocytes and development of diffuse cardiosclerosis.

Regenerative and plastic myocardial insufficiency characterized by impaired intracellular regeneration, progressive involution and apoptosis of cardiomyocytes associated with selective cardiotoxic effect of anthracycline antibiotic rubomycin is accompanied by enhanced proliferative and functional activities of fibroblasts and other stromal cells. Elimination of 30% cardiomyocytes and their atrophy are accompanied by the development of diffuse myocardial sclerosis, which is considered as a compensatory reaction of the connective tissue to the decrease in the weight of muscle fibers. Remodeling of the myocardium during anthracycline-induced cardiomyopathy due to changes in the parenchyma-stroma relationships does not lead to severe deformation of the heart, which is a favorable factor for normalization of myocardial architectonics after initiation of regenerative processes.

Animals↗

PubMed2001

Prenecrotic contracture damage in cardiomyocytes: photochemical fluorochrome staining and fluorescent microscopy of the myocardium.

Prenecrotic contracture changes in cardiomyocytes during ischemic and metabolic alteration of the myocardium are detected at the photooptic level by photochemical fluorochrome staining and examination in fluorescent light. Comparison of the fluorescent and polarization microscopic pictures of damaged cardiomyocytes showed relationships between optically active and isotropic constituents of the cell myofibrillar system. Contracture changes are determined by local mass redistribution in contractile compartments and transformations of the myofibril components, caused by protein structure coagulation in cardiomyocyte sarcomers.

Acute Disease↗

PubMed2001

Morphological characteristics of myocardial remodeling during compensatory hypertrophy in aging Wistar rats.

Remodeling of the myocardium in Wistar rats during aging is characterized by cardiomyocyte hypertrophy and increase of their total volume in the left ventricle; the total volume of the connective tissue also increases without marked changes in cardiomyocyte count and total volume of blood capillaries. The number of cardiomyocytes with contracture injuries of different severity in the myocardium of aging animals increases against the background of hemodynamic disorders. At the cellular level, compensatory hypertrophy of cardiomyocytes during aging is characterized by a pronounced increase in the myofibril bulk paralleled by relative deficiency of the mitochondria and pronounced deficiency of agranular sarcoplasmic reticulum and T system, involved in the regulation of intracellular Ca2+.

Aging↗

PubMed2001

Regenerative and plastic insufficiency of cardiomyocytes during impairment of protein synthesis.

Regenerative and plastic insufficiency of cardiomyocytes comprises cell changes resulting from impaired DNA-dependent RNA synthesis and biosynthetic processes. It is accompanied by progressive involution of cytoplasmic structures and causes atrophy and partial elimination of cells without signs of coagulation and colliquative necroses. Segregation and fragmentation of nucleoli in cardiomyocyte nuclei, lysis of myofibrils, and focal degradation of the cytoplasm are ultrastructural signs of impaired protein synthesis. Intracellular cardiomyocyte regeneration is characterized by disorientation of newly formed myofibrils and their excessive elongation, which are related to DNA damages followed by changes in transcription and translation in cardiomyocytes. Calculation of the absolute number of cardiomyocytes is a new approach to evaluation of contractile myocardial insufficiency.

Animals↗

PubMed2001

Ultrastructural changes in cardiomyocyte mitochondria during regenerative and plastic insufficiency of the myocardium.

Daunomycin-induced regenerative and plastic insufficiency of the myocardium was accompanied by accumulation of cardiomyocytes with unstable mitochondrial membranes containing enlarged mitochondria with lightened matrix and fragmented cristae. Total destabilization of mitochondrial membranes was found in cardiomyocytes with most pronounced ultrastructural signs of impaired protein synthesis. These changes in mitochondria were permanent, which suggested that swelling and destruction of cristae were related to intravital decrease in mitochondrial membrane stability.

Animals↗

PubMed2001

Ultrastructure of the contractile apparatus in cardiomyocytes during regenerative and plastic insufficiency of the myocardium.

Lytic changes in cardiomyocyte myofibrils constituting the morphological basis of contractile insufficiency were found in Wistar rats with regenerative and plastic myocardial insufficiency 3 h after daunomycin administration. Myofibrils became less dense, empty spaces appeared in many sarcomeres, sometimes total lysis of myofilaments within the sarcomere was noted. These changes were most pronounced in the perinuclear zone. Intracellular regeneration of cardiomyocytes was characterized by disorientation of newly formed myofibrils in relation to the long axis of muscle fibers and preserved myofibrils. Progressive inhibition of protein synthesis, lysis of myofibrils, and focal degradation of the sarcoplasm caused apoptotic death of some cardiomyocytes.

Animals↗

PubMed2001

Anthracycline-induced cardiomyopathy is manifested in decreased protein synthesis, impaired intracellular regeneration, and non-necrotic death of cardiomyocytes.

The cytostatic anthracycline antibiotic daunomycin hydrochloride led to the development of plastic myocardial insufficiency characterized by impaired intracellular regeneration of cardiomyocytes and progressive involution of cytoplasmic structures. Morphological signs of plastic myocardial insufficiency included fragmentation, annulation, or collapse of nucleoli in cardiomyocyte nuclei, lysis of myofilaments, sarcomeres, or myofibrils, focal degradation of the cytoplasm, and intensive autophagy. Fatal anthracycline-induced cardiac insufficiency was associated with massive cardiomyocyte loss due to their non-necrotic death and elimination. Our findings indicate that anthracycline-induced cardiomyopathy in laboratory animals is a convenient model for studying general mechanisms underlying the pathogenesis of regenerative and plastic cardiac insufficiency in humans.

Animals↗

PubMed2000

Instability of bronchial epithelium in chronic pulmonary diseases.

Pathomorphological examination of large bronchi in patients with occupational diseases, lung cancer, and in subjects exposed to radiation revealed structural and functional heterogeneity of the epithelium: the presence of focal atrophy, metaplasia, hyper- and dysplasia in the same biopsy specimen. This phenomenon was termed as instability of the epithelium. Thickness of the epithelium greatly varied, especially, in neoplastic processes. Atrophy and epithelial instability phenomenon are interpreted as morphological markers of ecological and oncological risk.

Autoradiography↗

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 of cardiomyocytes as extreme manifestation of regeneration and plastic insufficiency of myocardium.

Alkaline dissociation of the myocardium from rats with modeled anthracycline cardiomyopathy revealed decreased absolute number of cardiomyocytes, disturbances in their intracellular regeneration, although no sings of necrosis were observed. Regeneration and plastic insufficiency of the myocardium due to structural changes in the nuclei and disturbances in myofibril reproduction resulting from selective suppression of synthesis of contractile proteins in the cardiomyocytes leads to the death of up to 30% cardiomyocytes.

Animals↗