RESUMO
Five variants of myocardial lesions of different degree were simulated in experiments on 8 dogs, 61 rabbits and 30 rats, namely micronecrosis, diffuse myocarditis, focal dystrophy, small- and large-focal myocardial infarction. The experimental models of heart lesions can be used for studying the pathophysiological mechanisms in cardiac pathology and evaluation of the therapeutic efficacy of new drugs in experimental pharmacology.
Assuntos
Cardiomiopatias/induzido quimicamente , Modelos Animais de Doenças , Animais , Cardiomiopatias/tratamento farmacológico , Cães , Avaliação Pré-Clínica de Medicamentos , Eletrocardiografia , Feminino , Masculino , Infarto do Miocárdio/induzido quimicamente , Infarto do Miocárdio/tratamento farmacológico , Miocardite/induzido quimicamente , Miocardite/tratamento farmacológico , Miocárdio/patologia , Necrose , Coelhos , RatosRESUMO
In dogs, pituitrin increases, and isadrin reduces, the tonicity of coronary arteries. Successive administration of the two agents to rabbits causes functional and metabolic unbalance of the heart, with resultant myocardial necrotic foci in the presence of blood hypercoagulation and heart muscle contractility disordered. The disorder of cardiomyocyte stereo architectonics is an essential element of the pathophysiologic mechanism of small-focal myocardial infarction.
Assuntos
Contração Miocárdica , Infarto do Miocárdio/fisiopatologia , Miocárdio/metabolismo , Nucleotídeos de Adenina/metabolismo , Animais , Coagulação Sanguínea , DNA/metabolismo , Cães , Feminino , Masculino , Mitocôndrias Cardíacas/metabolismo , Infarto do Miocárdio/metabolismo , Infarto do Miocárdio/patologia , Miocárdio/ultraestrutura , Fosforilação Oxidativa , RNA/metabolismo , CoelhosRESUMO
Experiments on 107 rabbits and 76 white rats with the use of electrophysiological, biochemical and electron microscopy research methods have shown that nonachlazine-induced improvement of heart contractility in microfocal myocardial infarction occurs as a result of the shortening of the systolic and lengthening of the diastolic phases of the heart cycle. Nonachlazine improves the processes of oxidative phosphorylation in heart mitochondria in myocardial infarction, which is accompanied by inhibition of the activity of succinate dehydrogenase and transition of oxidation from succinate to NAD-dependent substrates.
