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Journal of Third Military Medical University ; (24)2003.
Artigo em Chinês | WPRIM | ID: wpr-678478

RESUMO

Objective To study the reversion of the metabolic gene expression pattern of hypertrophic cardiac and role of Carvedilol and to explore the molecular regulatory mechanism of Carvedilol on attenuating the reversion back towards fetal energy metabolism occurring with the development of cardiac hypertrophy. Methods A model of hypertrophy induced by coarctation of abdominal aorta(CAA) in male Wistar rats was employed and changes of parameters such as hemodynamics, ventricular remodeling parameters, free fatty acid in blood serum and cardiac myocyte and expressions of muscle carnitine palmitoyltransferase Ⅰ (M CPT Ⅰ) and medium chain acyl CoA dehydrogenase (MCAD) mRNA were investigated in the experimental animals in operation group(CAA), sham operation group(SH) and Carvedilol intervention group(CAR) at 16 weeks after operation. Results Significant hypertrophy was found in the left ventricle in CAA group(3.41?1.30 vs 2.46?1.31, P

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