Barbosa Marcos E, Alenina Natalia, Bader Michael
Max-Delbrück-Center for Molecular Medicine, Berlin-Buch, Germany.
Methods Mol Med. 2005;112:339-52. doi: 10.1385/1-59259-879-x:339.
Myocardial hypertrophy is an adaptational process of the heart to increased workload caused by mechanical stress, growth factors, cytokines, catecholamines, or primary genetic abnormalities. Chronic induction of hypertrophy leads to the gradual deterioration of ventricular function and is an independent risk factor for cardiac-related morbidity and mortality in patients with hypertension and ventricular arrythmias. Transgenic animals are very useful models to study the factors involved in the pathogenesis of cardiac hypertrophy. To achieve this goal, rodents lacking or overexpressing a specific gene are subjected to banding of the abdominal aorta, an experimental model of cardiac hypertrophy that leads to pressure overload on the heart. After periods between 3 and 21 d, parameters such as cardiac hemodynamics, morphologic alterations, and expression of marker genes (e.g., the gene for atrial natriuretic peptide) are analyzed in genetically modified animals and compared with controls elucidating a possible implication of the modified gene in the pathogenic process leading to myocardial hypertrophy. This article summarizes the techniques necessary to induce left ventricular hypertrophy by aortic banding and to analyze the effects of this experimental model on hemodynamics, cardiac morphology, and gene expression of transgenic and control animals.
心肌肥大是心脏对由机械应力、生长因子、细胞因子、儿茶酚胺或原发性基因异常引起的工作量增加的一种适应性过程。慢性肥大诱导会导致心室功能逐渐恶化，并且是高血压和室性心律失常患者心脏相关发病率和死亡率的独立危险因素。转基因动物是研究参与心脏肥大发病机制的因素的非常有用的模型。为实现这一目标，对缺乏或过表达特定基因的啮齿动物进行腹主动脉结扎，这是一种心脏肥大的实验模型，会导致心脏压力过载。在3至21天的时间段后，在转基因动物中分析诸如心脏血流动力学、形态学改变和标记基因（例如心房利钠肽基因）表达等参数，并与对照进行比较，以阐明修饰基因在导致心肌肥大的致病过程中的可能作用。本文总结了通过主动脉结扎诱导左心室肥大以及分析该实验模型对转基因和对照动物的血流动力学、心脏形态和基因表达的影响所需的技术。
