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- Objective To evaluate the effect of perindopril on ventricular tachycardia in rabbits with cardiac hypertrophy. 目的观察培垛普利对兔肥厚心肌室性心律失常的保护作用。
- Background The childhood onset of idiopathic cardiac hypertrophy that occurs without a family history of cardiomyopathy can portend a poor prognosis. 背景：儿童时期特发性肥厚性心肌病无心肌病家族病史，预示着预后不良。
- The exogenous BH4 on blood pressure,myocardial ischemia/reperfusion injury and cardiac hypertrophy has significant effect. 给予外源性的BH4对高血压、心肌缺血/再灌注损伤和心肌肥厚有明显的治疗作用。
- However,in spite of the effect of lowering blood pressure,hydralazine did not prevent or regress cardiac hypertrophy and did not decrease the level of p-ERK and BNP in SHR. 而降压效果相似的肼苯哒嗪不能抑制心肌肥厚，对p-ERK和BNP水平没有影响，提示BNP水平可以反映逆转心肌肥厚药物疗效。
- Ultimately, knockout mice deeloped cardiac hypertrophy and heart failure, which inoles protein kinase C signal transduction but not the mitogen-actiated protein kinase pathway. 最终结果是基因敲除小鼠心脏发生肥厚和心衰，与蛋白激酶C信号转导有关而与丝裂原激活蛋白激酶途径无关。
- Reactive oxygen species can mediate signalling pathways in cardiac hypertrophy and cardiomyocyte apoptosis, and lead to endothelial dysfunction by inactivating nitrogen monoxide. 活性氧通过信号通路介导心肌细胞肥大和凋亡;通过灭活一氧化氮等机制导致内皮功能紊乱。
- In the process of external aldosterone inducing cardiac hypertrophy, the activity of calcineurin increases and the expression of its negative-control factor, the expression of Cain, also increased. 在外源性醛固酮诱发大鼠发生心肌肥厚反应过程中,钙调神经磷酸酶的活性增加,而其内源性负性调节蛋白钙调神经磷酸酶抑制因子的表达亦相应增加;
- Peroxisome proliferator-activated receptor(PPAR) is a transcription factor,belongs to the nuclear receptors family,plays a critical role in the pathophysiology of cardiac hypertrophy. 过氧化物酶体增殖激活受体(PPAR)是甾体激素受体超家族的新成员,能被脂肪酸以及外源性过氧化物酶体增殖剂激活,而调控参与脂类代谢的某些酶的基因表达。
- Cardiac hypertrophy and extracellular matrix remodeling happened as a result of chronic overrange of pressure in heart and hypervolaemia which lead to damage of relaxation and compliance of heart. 主要表现为心脏在慢性超负荷的压力、容量作用下发生的病理改变致使左室肥厚组织胶原结构发生改变,导致心肌顺应性降低,舒张功能受到损害;
- Objective To create the exercise-induced physiological and DOCA-salt-induced pathological cardiac hypertrophy animal model,and evaluate cardiac function during development of hypertrophy. 目的通过建立运动引起的生理性心脏肥大和DOCA高盐引起的病理性心脏肥大大鼠模型,比较评价两种心脏肥大时心脏功能情况。
- It is known that neurohumoral factors and mechanical loads play important roles in the cardiac remodeling process, with the later having extremely great impact on cardiac hypertrophy. 目前已知神经体液性因素与机械性压力在心脏重塑过程中扮演著重要角色，其中机械性压力对心脏肥大的产生更是有著关键性的影响。
- For instance, the mouse model of obesity may fail to represent the important features of obesity in human including hypertension, hyperlipidemia, hyperinsulinemia and cardiac hypertrophy. 更重要的是，家兔脂蛋白的特征与人相似，脂蛋白代谢更适合于人类血管生物学（如，动脉粥样硬化）研究。
- Molecular Pathways in Cardiac Hypertrophy Unraveled 发现心脏肥厚的分子途径
- Cardiac hypertrophy is the consequence of hypertrophic stimulus-induced changes in gene expression,which is linked by intracellular signal transduction. 心肌肥厚是肥大刺激诱导核内基因异常表达的结果，细胞内信号转导通路是肥大刺激与核内基因转录活化的偶联环节。
- compensatory cardiac hypertrophy 代偿性心脏肥大
- A STUDY OF THE EFFECT OF PTEN ON CARDIAC HYPERTROPHY PTEN在心肌肥厚中的作用初探
- Masked Hypertension in Children May Precede Cardiac Hypertrophy 儿童隐性高血压可能引起心脏肥厚
- Keywords Calcineurin;Cardiac hypertrophy;Signal pathway; 钙调神经磷酸酶;心肌肥大;信号通路;
- Keywords Ascending aorta;Cardiac hypertrophy;Mouse;Transgene; 关键词升主动脉;心肌肥厚;小鼠;转基因;
- Keywords isoproterenol;cardiac hypertrophy;berberine;rat; 异丙肾上腺素;心肌肥厚;黄连素;大鼠;
