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1.
Rio de Janeiro; s.n; 2009. 113 p. ilus.
Thèse Dans Portugais | LILACS | ID: lil-564731

Résumé

A insuficiência cardíaca (IC) é a evolução final das várias formas de doenças cardiovascular, sendo resultado de modificações estruturais, metabólicas e de contratilidade miocárdica. A fim de compreender o papel na dinâmica do metabolismo cardíaco no estado basal e na sobrecarga de pressão, utilizamos os modelos de cre-lox com deleção específica no coração para substrato do receptor de insulina (IRS) e co-ativador do PPAR (PGC-1b) e analisamos a estrutura cardíaca (histologia e estereologia), função cardíaca (ecocardiograma e técnica de Working heart), o metabolismo (isolamento de cardiomiócito e captação de glicose), ação hormonal (Western Blotting), expressão gênica (PCR-RT) de enzimas do metabolismo (lipídico, glicídico, da cadeia respiratória fatores transcricionais e hipertróficos) e a função mitocondrial. Verificamos, nos CIRS12KO, disfunção cardíaca grave, disfunção mitocondrial e prejuízo na expressão gênica das enzimas do metabolismo energético. Nos PGC-1BKO observamos disfunção mitocondrial e alteração de expressão gênica das enzimas do metabolismo energético quando submetidos à sobrecarga de pressão. Através do estudo do metabolismo cardíaco e da expressão gênica nestes diferentes modelos conseguimos explorar as vias metabólicas que levam a hipertrofia compensada à IC. Sugerimos que o mecanismo responsável pela descompensação seja a disfunção mitocondrial em conseqüência à alteração da expressão gênica. E que IRS e o PGC-1B são fatores chaves da dinâmica cardíaca, e que são indispensáveis para a estrutura e funcionamento cardíaco. Além de representar alvo promissor para limitar a transição de hipertrofia cardíaca compensada a insuficiência cardíaca...


Heart failure (HF) is the end stage of different types of cardiovascular diseases and it is characterized by changes in the metabolic and myocardial contractility. We use the models cre-lox with specific knockout for insulin receptor substrate (IRS) and co-activator of PPAR (PGC-1b) (basal and pressure overload). The objective was understood the role in the dynamics of cardiac metabolism. We analyzed cardiac structure (histology and stereology), cardiac function (echocardiography and the working heart technique), metabolism (glucose uptake), hormonal action (Western Blotting), gene expression (RT-PCR) from enzyme metabolism (lipid, carbohydrates, respiratory chain, transcriptional and hypertrophic factors) and mitochondrial function. We found in CIRS12KO, severe cardiac dysfunction, mitochondrial dysfunction and reduction of gene expression. And in the PGC-1bKO when subjected to pressure overload, the progression to heart failure, with mitochondrial dysfunction, and alteration of gene expression from enzyme metabolism. The data show that changes on cardiac metabolism and gene expression in both models explain the metabolic pathways that lead to compensated hypertrophy to HF. We suggest that the mitochondrial dysfunction and the gene expression was possible mechanisms for HF. We conclude that IRS and PGC-1b are key factors of cardiac dynamics, which are essential to the structure and heart function. IRS and PGC-1b represent a promising target for limiting the transition from compensated cardiac hypertrophy to heart failure...


Sujets)
Animaux , Rats , Cardiomégalie/complications , Expression des gènes/génétique , Défaillance cardiaque/étiologie , Défaillance cardiaque/anatomopathologie , Souris , Mitochondries du myocarde/métabolisme , Mitochondries du myocarde/anatomopathologie , Récepteur PPAR bêta/usage thérapeutique , Substrats du récepteur à l'insuline/génétique , Substrats du récepteur à l'insuline/métabolisme , Souris knockout
2.
Journal of Forensic Medicine ; (6): 107-112, 2005.
Article Dans Chinois | WPRIM | ID: wpr-983083

Résumé

OBJECTIVE@#To observe ultra-structural pathological changes of materiality viscera of rats poisoned by different dose of tetramine and to study the toxic mechanism.@*METHODS@#Acute and subacute tetramine toxicity models were made by oral administration with different dose of tetramine. Brain, heart, liver, spleen and kidney were extracted and observed by electromicroscopic examination.@*RESULTS@#The injuries of brain cells, cardiocytes and liver cells were induced by different dose of tetramine. These were not obviously different of the injuries of the kindy cells and spleen cells of rats poisoned by different dose of tetramine. Ultra-structural pathological changes were abserved including mitochondria slight swelling and neurolemma's array turbulence in the brain cells, mitochondria swelling or abolish and rupture of muscle fiber in the heart cells, mitochondria swelling and the glycogen decreased in the liver cells.@*CONCLUSION@#The toxic target organs of tetramine are the heart, brain and liver.


Sujets)
Animaux , Femelle , Mâle , Rats , Encéphale/anatomopathologie , Composés pontés/intoxication , Relation dose-effet des médicaments , Foie/anatomopathologie , Microscopie électronique à transmission , Mitochondries du myocarde/anatomopathologie , Mitochondries du foie/anatomopathologie , Myocarde/anatomopathologie , Intoxication/anatomopathologie , Rat Sprague-Dawley
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