Objective To investigate the mechanism of reversion of myocardial interstitial fibrosis in diabetic cardiomyopathy (DCM) by valsartan.
目的探讨缬沙坦逆转糖尿病心肌病(DCM)心肌间质纤维化的作用机制。
ACEI reduces the levels of ACEmRNA directly and significantly inhibits the progression of myocardial interstitial fibrosis and cardiac remodeling.
臼acei可直接下调ace测a表达，有效地抑制了心肌间质纤维化，阻止心肌重塑的发生。
CONCLUSION: Myocardial interstitial fibrosis and the reduction of myofibril elements are the major pathological basis for the impairment of cardiac function in patients with DCM.
结论：DCM患者心肌间质纤维化，肌原纤维减少是扩张型心肌病心功能损害的主要病理基础。
CONCLUSION Fluvastatin could inhibit myocardial interstitial fibrosis and improve the cardiac function of diabetic rats, which might be related to the down-regulating of the CTGF expression.
结论氟伐他汀可逆转糖尿病大鼠心肌间质纤维化并改善心功能，这种作用可能与其抑制CTGF的表达有关。
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.
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。
Myocardial fibrosis is caused by overdeposition of myocardial interstitial collagen and proportion disorder of all kinds of collagen, and it occurs in many heart diseases.
心肌纤维化是由于心肌间质胶原沉积增多，各型胶原比例失调所导致，可发生于多种心血管疾病。
The abnormal accumulation of interstitial collagen and myocardial fibrosis could destroy the network structure of myocardial interstitium.
并能使心肌组织电的各向异性增加，容易引起心律失常，甚至猝死。
In he stain, myocardial hypertrophy, severe myolysis and extensive fibrosis in the interstitial space of the atria were found in AF group.
HE染色发现心房颤动患者的心房有肌溶解、心肌肥厚及广泛的间质纤维化改变。
In he stain, myocardial hypertrophy, severe myolysis and extensive fibrosis in the interstitial space of the atria were found in AF group.
HE染色发现心房颤动患者的心房有肌溶解、心肌肥厚及广泛的间质纤维化改变。
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