高血压引起心脏的压力负荷增大， 从而导致心肌肥大。
The hypertension creates a greater pressure load on the heart to induce the hypertrophy .
而后天性心脏病的心肌肥大是多离子通道病变而非特殊性。
In contrast it is characterised with multi-channels and nonspecific disorder in the hypertrophied myocardium in the acquired heart disease.
目的：探讨一气化氮在压力超负荷心肌肥大反应过程中的作用。
Objective: To study the role of nitric oxide in myocardial hypertrophy caused by pressure overload in rats.
目的：研究运动性心肌肥大形成中血浆生物活性肽的含量及意义。
Objective:To investigate the changes of plasma biological active peptides in exercise-induced cardiac hypertrophy in rats.
资料综合：在持续性运动期间运动诱导心肌肥大是心输出量增加的生理基础。
DATA SYNTHESIS: During continuous exercise, myocardium hypertrophy induced by exercise was the physical basis of the increase in cardiac output.
目的探讨丝裂素活化蛋白激酶(MAPK)在肾性高血压致心肌肥大中的作用。
Objective to investigate the effect of mitogen-activated protein kinase (MAPK) on pathogenesis in myocardium hypertrophy of renal hypertension rats.
因此，探讨心肌肥大的发生机制、寻求合理的防治措施具有重要的理论及实践意义。
It is important to discover mechanisms of LVH and to find preventive measures, which have significance in the field of both theoretic studies and clinical practice.
本研究提示运动性心肌肥大的心肌抗缺血再灌注损伤的能力较高血压心肌肥大者增强。
It suggested that the ability of anti-injury in exercise-induced cardiac hypertrophy is higher than that in hypertension.
本研究室的主要研究方向为心肌肥大时的细胞信号转导通路及脂联素对心脏功能的影响。
The main interest of the laboratory is focused on the signal transduction pathway during cardiac hypertrophy and the effect of adiponectin on cardiac function.
运动心脏学已成为一门新兴的交叉学科，本文就运动心脏学的基础研究、运动性心肌肥大；
Sports Cardiology has become anew overlapping school subject is paper presents a discussion about basic research on Sports Cardiology, motional myocardial Hypertrophy;
腹部超声示肝硬化、门脉高压和巨脾，超声心动图示心肌肥大、二尖瓣和三尖瓣轻度关闭不全；
Abdominal ultrasound examinations showed cirrhosis, portal hypertension, splenomegaly. Echocardiogram showed left ventricular myohypertrophia, mild mitral and tricuspid valve insufficiency.
分析运动诱导心脏血流动力学的变化和心肌肥大有助于区分病理性心肌肥大，为运动健身提供依据。
To analyze that the changes of heart hemodynamics induced by exercise and myocardium hypertrophy are helpful to differ the pathologic myocardium hypertrophy and provide evidence for exercise.
目前，对运动性心肌肥大属于调节性、生理性肥大的认识渐趋一致，但其发生机制尚未完全阐明。
At present , the recognization is agreed on that cardiac hypertrophy belongs to regulatory and physical cardiac enlargement. But its mechanisms are still not be stated clearly.
目的：为探讨长期运动训练与高血压病引起的心肌肥大在功能方面的差别，对两者进行心肌力学的分析。
Making myocardial mechanics researches on it contribute to bring to light the differences and connections between this two kinds of myocardial hypertrophy.
背景与目的：心肌肥大是多种心血管疾病的共同病理过程，是导致心原性死亡的最重要的病理基础之一。
Background and Objective: Cardiac hypertrophy serves as a common pathway in various cardiovascular diseases. It is one of the most important pathological foundations resulting in cardiogenic death.
结果提示：MI早期随着非梗塞心肌肥大的建立，肌球蛋白atp酶活性及其同功酶分布也发生了适应性的改变。
It is suggested that with the development of myocardial hypertrophy in early stage of MI, adaptive changes in myosin ATPase activity and isoenzyme distribution occur.
仅从运动性心肌肥大的生物学机制方面，就诱导其发生的刺激因素及其信号转导通路、基因表达等几个方面加以综述。
In this article we only reviewed the biological mechanism of exercise induced cardiac hypertrophy by its inductive stimulus, pass way for signal transduction and genetic expression.
结论：环孢霉素A可抑制高血压心肌肥大，但较大剂量或较长时间应用则会产生严重心肌水肿，并且这种作用是剂量、时间依赖性的。
CONCLUSION: CsA can inhibit hypertensive cardiac hypertrophy, but large dose or longer period of application will lead to severe myocardial edema, which is dose-dependent and time-dependent.
这些结果说明，细胞成份的自体吞噬降解在心肌肥大过程中起着重要调节作用，扩张的T管也反映了心肌细胞外吐加快的适应性改变。
These results suggest that autophagy of cellular elements seems to play an important regulative role in hypertrophied process and dilated T-tubules actually reflect myocardial adaptive changes.
心肌细胞肥大是一种多因素参与调节的复杂的动态过程。
The cardiac muscle cell hypertrophy is a complicated dynamic process with many regulation factors to participate in.
目的：探讨心肌矢量应变技术在检测扁桃体腺样体肥大患儿心脏功能方面的应用价值。
OBJECTIVE: to study the value of Xstrain technology in the evaluation of cardiac function in children with tonsil adenoidal hypertrophy.
但近来有研究表明，PTEN与细胞的体积大小有密切关系，尤其是神经元和心肌细胞肥大。
More recently, it has been found that PTEN is closely related to cell size, especially to neuron enlargement and cardiomyocyte hypertrophy.
结论辛伐他汀能够抑制血清诱导的心肌细胞肥大，升高pten表达水平可能是其分子生物学机制之一。
Conclusion Simvastatin can inhibit the hypertrophy of cultured rat cardiac myocytes induced by serum, the mechanism of which might be related with the increase of PTEN expression.
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。
Reactive oxygen species can mediate signalling pathways in cardiac hypertrophy and cardiomyocyte apoptosis, and lead to endothelial dysfunction by inactivating nitrogen monoxide.
本文从心肌细胞肥大这个角度阐述阿托伐他汀对心室重塑的影响。
In this text, we reviewed the effect of atorvastatin on the treatment of cardiac myocyte hypertrophy.
该生长因子响应力学刺激而表达，现有研究表明其具有促进肌肉肥大、心肌保护以及神经修复等作用。
Further studies found that MGF could promote muscle hypertrophy, preserve cardiac muscle and repair the damage of nerves.
结论：GH可使心肌细胞、骨骼肌细胞肥大而不是间质组织增生。
Conclusion GH can induce hypertrophy of cardiac muscle cells and skeletal muscle cells but not interstitial proliferation.
结论慢性心衰时左心房心肌细胞为以宽度增加为主的肥大性生长。
Conclusion For chronic heart failure cardiac muscle cells of left atrium was characterized by hypertrophic growth of width increase.
结果表明肝硬化存在心肌间质纤维化和肥大细胞浸润，可能参与肝硬化心肌病的发生。
Electromicroscopy pointed to myocardial interstitial fibrosis and MC infiltration, whose presence in cirrhotic myocardium may have played a role in the pathogenesis of cirrhotic cardiomyopathy.
严重的高血压，并且多年未经治疗，引起左心室显著地肥厚。心肌纤维已过度肥大。
The left ventricle is markedly thickened in this patient with severe hypertension that was untreated for many years. The myocardial fibers have undergone hypertrophy.
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