Toxic liver injury with the development of fibrosis and cirrhosis was modeled in Wistar rats by intragastric administration of 0.1 ml/kg CCl4 in combination with 5% ethanol with glucose 3 times a week for 6 weeks. The animals were treated with betulonic acid amide (50 mg/kg in Tween aqueous solution) and heptral (6 mg/kg) as hepatoprotective compounds. It was found that betulonic acid amide stimulated the regenerative response in hepatocytes under conditions of combined toxic exposure and promoted recovery of their qualitative and quantitative characteristics, which was accompanied by a significant decrease in the severity of liver fibrosis and the absence of cirrhotic transformation of the liver.

The changes in mammary gland bioimpedance were examined in the dynamics of the inflammatory process. Bioimpedance of affected gland was 2-3-fold lower than that of the contralateral one; normally, this difference did not exceed 10%. The phases of inflammation development were paralleled by changes in bioimpedance. During wound epithelization, impedance increased and approximated the normal level. Further increase of bioimpedance by more than 30% and its stabilization at this level attested to recurrence of inflammation, while its irreversible drop indicated devitalization the tissues. The diagnostic criterion attesting to the development of local inflammatory reaction is deviation of bioimpedance in the impaired area by more than 15% from that of the adjacent intact site.

Here we describe an experimental tumor, hepatocarcinoma-29: transplantable strain of this tumor is maintained in an ascitic form in CBA/LacYIcgn mice in Institute of Cytology and Genetics of SD of RAS. After inoculation into the thigh muscles, the tumor induces anorexia, progressing loss of fat and muscle tissues, and physiological changes specific for cachexia: leukocytosis, hypoglycemia, and hypercorticism. The tumor metastasizes to all vital viscera and leads to animal death from renal failure.

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.