心肌肥厚

因此，ox-LDL除了有致动脉粥样硬化作用，还可能诱导心肌肥厚。

Hence , in addition to atherogenic effects , ox-LDL may also affect cardiac myocytes leading to myocardial hypertrophy .

结论肥胖组儿童存在的肾素-血管紧张素-醛固酮系统（RAAS）异常激活在引起其心肌肥厚中起作用。ALD与AngⅡ相互作用，增强了RAAS的活性，促进心肌肥厚的进一步发展。

Conclusion The abnormal activation of renin-angiotensin-aldosterone system ( RAAS ) exerts an effect on myocardial hypertrophy in simple adipose children .

结论：（1）NF-κB参与了高血压心肌肥厚的形成。

Conclusions : ( 1 ) NF - κ B contributes to the formation of LVH of hypertension .

结果：术后2、6、12周心肌肥厚组大鼠心肌组织糜酶样活性较同期正常对照组显著增高（P＜0.01）；

Results : It was found that the myocardial chymase like activity increased markedly in hypertrophied rat ( 2,6,12 weeks );

cDNA芯片法筛选压力负荷型心肌肥厚相关基因

Identification of genes related to mechanical load-induced cardiac hypertrophy by cDNA chip

大鼠心肌肥厚时心脏心钠素、ras癌基因的表达

Expression of ANP and ras gene in myocardiac hypertrophy of rats

心肌肥厚大鼠心肌细胞核体外转录活性和RNA核孔转出的变化

Changes of transcription activity and RNA export of myocardial nuclei in vitro in pressure overload-induced rat hypertrophic heart

健康雄性SD大鼠150只，随机分为手术组和对照组，采用腹主动脉缩窄法建立心肌肥厚模型。

The cardiac hypertrophy model of rat was prepared by transverse aortic coarctation ( TAC ) .

结论（1）ADM可能既是循环激素，又是自分泌和／或旁分泌激素，在心肌肥厚发生发展中起代偿作用，有望成为评价心肌肥厚严重程度的新的敏感指标。

Conclusion ( 1 ) ADM was probably a circulating hormone .

方法：大鼠腹腔注射NE建立心肌肥厚模型；

METHODS : Left ventricular hypertrophy was induced by injecting ME intraperitoneally in rats .

EGCG抑制心肌肥厚胶原生成和细胞增殖

EGCG inhibition against collagen accumulation and cell proliferation in cardiac hypertrophy

压力超负荷性心肌肥厚大鼠心肌ADM、ET、ANP变化的实验研究

Experimental study on the changes of ADM , ET and ANP in rats with pressure overload myocardial hypertrophy

创新点1.建立了ox-LDL诱导心肌肥厚模型。

Ox-LDL-induced cardiac hypertrophy model has been established . 2 .

目的：探讨豚鼠慢性充血性心力衰竭（CHF）及致心肌肥厚的动物模型制作方法。

Objective : To investigate the animal model of guinea pig chronic heart failure and compensatory hypertrophy .

说明TGFβ1表达可能是介导人体超负荷性心肌肥厚发生的因素之一。

TGF β _1 , mRNA and protein expression may play a role in the mechanism of human heart hypertrophy induced by overload .

目的探讨牛磺酸对肾血管性高血压大鼠心肌肥厚及组织局部肾素-血管紧张素系统（RAS）的影响。

Objective To investigate the role of taurine on cardial hypertrophy and local renin-angiotensin system in renovascular hypertensive rats .

结论在心肌肥厚性重构患者中，与LVEF比较，MAD能更早地反映患者的左室收缩功能减退情况。

Conclusion MAD can evaluate left ventricular dysfunction earlier than LVEF in patients with cardiac hypertrophic and remodeling .

结论：原发性高血压与肾性高血压的心肌肥厚均与PP、BVP相关，提示PP、BPV可能是心肌肥厚的预测因子；

Conclusion : PP and BPV may be the predict factors of LVMI in hypertension patients .

辛伐他汀对压力超负荷大鼠APN、IL-6及心肌肥厚影响

Effect of simvastatin on serum adiponectin , interleukin-6 and cardiac hypertrophy induced by pressure overload in rats

Rho激酶抑制剂对压力超负荷性大鼠心肌肥厚的影响

Role of Rho Kinase Inhibitor in Pressure Overload Induced Cardiac Hypertrophy in Rats

目的探索心肌肥厚与Wnt信号途径活化的关系。

AIM To observe the relation between cardiac muscle hypertrophy and Wnt signal pathway .

钠尿肽（natriureticpeptides，NPs）是一组具有利钠、利尿、舒血管和抗细胞增殖效应的多肽，具有抗心力衰竭、心肌肥厚和移植血管再狭窄的重要作用。

Natriuretic peptides ( NPs ) are a family of polypeptides possessing natriuretic , diuretic , vasodilative and anti-proliferation actions .

压力超负荷心肌肥厚过程中血清TNF-α、IL-1β、IL-6的变化

Changes in Serum TNF - α, IL - 1 β and IL - 6 in the Whole Course of Over - loaded Heart Hypertrophy

阿托伐他汀对ApoE基因缺陷小鼠心肌肥厚一级预防的实验研究

Primary prevention effect of atorvastatin on myocardial hypertrophy in ApoE-deficient ( ApoE - / - ) mice

结论运动诱导的心肌肥厚使QT离散度减小，反映了长期运动个体心肌复极化的稳定性。

Conclusion QTd was decreased in exercise-induced cardiac hypertrophy subjects , which may reflect homogeneous myocardial repolarization in long term trained subjects .

大鼠压力负荷性心肌肥厚时心脏RAS的变化。

Cardiac RAS and myocardial hypertrophy : The pressure overload myocardial hypertrophy was induced in rats by abdominal aortic banding for 6 weeks .

探讨压力负荷增高性心肌肥厚时心肌胶原网络及心肌细胞外基质金属蛋白酶（MMPs）活性的变化。

To examine changes of collagen network and Matrix Metaloproteinases ( MMPs ) activity in hypertrophied rat myocardium .

ACEI和ARB对预防和治疗心肌肥厚有一定的作用，且两药合用作用好于单独应用。

ACEI and ARB may have the positive importance in the treatment and prevention of LVH .

心电图异常以ST-T改变为常见，其次分别为心律失常、心肌肥厚等。

ECG abnormalities with ST-T change the common , followed by arrhythmia , such as cardiac hypertrophy .

结论：IGF-1可能参与了HCM心肌肥厚的发生发展过程。

Conclusion : the increased serum IGF-1 may be involved in the occurance and development of HCM associated LVH .