Héliès-Toussaint Cécile, Moinard Christophe, Rasmusen Carole, Tabbi-Anneni Imène, Cynober Luc, Grynberg Alain
INRA UR 1154 LMFC, Faculté de pharmacie, 5, rue J. B. Clément, F-92290 Châtenay Malabry France.
Am J Physiol Regul Integr Comp Physiol. 2005 May;288(5):R1325-31. doi: 10.1152/ajpregu.00320.2004. Epub 2005 Jan 6.
Heart failure is a severe pathology, which has displayed a dramatic increase in the occurrence of patients with chronic heart disease in developed countries, as a result of increases in the population's average age and in survival time. This pathology is associated with severe malnutrition, which worsens the prognosis. Although the cachexia associated with chronic heart failure is a well-known complication, there is no reference animal model of malnutrition related to heart failure. This study was designed to evaluate the nutritional status of rats in a model of loss of cardiac function obtained by ascending aortic banding. Cardiac overload led to the development of cardiac hypertrophy, which decompensates to heart failure, with increased brain natriuretic peptide levels. The rats displayed hepatic dysfunction and an associated renal hypotrophy and renal failure, evidenced by the alteration in renal function markers such as citrullinemia, creatininemia, and uremia. Malnutrition has been evidenced by the alteration of protein and amino acid metabolism. A muscular atrophy with decreased protein content and increased amino acid concentrations in both plasma and muscle was observed. These rats with heart failure displayed a multiorgan failure and malnutrition, which reflected the clinical situation of human chronic heart failure.
心力衰竭是一种严重的病理状况，在发达国家，由于人口平均年龄和生存时间的增加，慢性心脏病患者的发病率急剧上升。这种病理状况与严重营养不良相关，而营养不良会使预后恶化。尽管与慢性心力衰竭相关的恶病质是一种众所周知的并发症，但目前尚无与心力衰竭相关的营养不良的动物模型。本研究旨在评估通过升主动脉缩窄获得的心功能丧失模型中大鼠的营养状况。心脏负荷过重导致心脏肥大，进而失代偿为心力衰竭，同时脑钠肽水平升高。大鼠出现肝功能障碍以及相关的肾萎缩和肾衰竭，这通过肾功能标志物如瓜氨酸血症、肌酐血症和尿毒症的改变得以证实。蛋白质和氨基酸代谢的改变证明了营养不良的存在。观察到肌肉萎缩，血浆和肌肉中的蛋白质含量降低，氨基酸浓度升高。这些心力衰竭大鼠表现出多器官功能衰竭和营养不良，反映了人类慢性心力衰竭的临床情况。
