Biomedical subjects

E L Lushnikova

Publications and source records attributed to E L Lushnikova.

At least 19 recordsLinked to original sources

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

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

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↗

PubMed2000

Peculiarities of intracellular regeneration of cardiomyocytes during plastic myocardial insufficiency.

We performed morphological assay of the myocardium in Wistar rats with anthracycline cardiomyopathy and SHR rats with genetically determined arterial hypertension causing hypertrophic cardiomyopathy. Both disorders were accompanied by a decrease in protein synthesis and development of plastic cardiomyocyte insufficiency. Electron microscopy revealed peculiarities of intracellular regeneration of cardiomyocytes. We observed disorientation of newly formed myofibrils lying between preserved myofibrils. These myofibrils were positioned perpendicular or at angle to the long axis of muscle fibers, or extended from the Z line (in a fan-like manner) crossing each other. Regeneration disturbances also included excessive elongation of myofibrils. These abnormalities of myofibril regeneration were related to changes in transcription and translation in cardiomyocytes, due to DNA damages caused by cardiotoxic doses of rubomycin.

Animals↗

PubMed2000

Focal degradation of cytoplasmic organelles in cardiomyocytes during regenerative and plastic myocardial insufficiency.

Focal degradation of cardiomyocyte ultrastructures and cytoplasm, their sequestration, and autophagy were found in Wistar rats with daunomycin-induced regenerative and plastic myocardial insufficiency starting from day 1 after cytostatic treatment. These changes were morphologically manifested in the formation of myelin-like structures, autophagosomes, and secondary lysosomes. Sequestration and partial autophagy of the cytoplasm in cardiomyocytes with diminished or blocked protein synthesis reflect cell regression or involution directed to the adjustment of the cytoplasm volume to functional state of the nucleus.

Animals↗

PubMed2000

Ultrastructure of nuclear compartment in cardiomyocytes during regenerative and plastic insufficiency of the myocardium.

We studied ultrastructure of nuclear compartment in cardiomyocytes during regenerative and plastic insufficiency of the myocardium induced by anthracycline antibiotic daunomycin. A peculiarity of ultrastructural organization of cardiomyocyte nuclei under these conditions is almost complete disappearance of the heterochromatin lumps. The earliest changes in nucleoli under conditions of disturbed DNA-dependent RNA synthesis are segregation of the granular and fibrillar nucleolonema components. Deep alterations in the nucleoli manifested by fragmentation and annulation correlate with pronounced changes in cardiomyocytes ultrastructure, intensive lysis of the myofilaments, reduction of the organelles, and enhanced autophagocytosis.

Animals↗

PubMed1999