摘要
目的 探讨血管紧张素II及其I型受体在扩张型心肌病心室间质胶原重塑中的作用。方法 用呋喃唑酮饲养Wistar大鼠建立扩张型心肌病大鼠模型 ,超声心动图检测大鼠心功能 ,病理学测量大鼠左室内径和左游离壁厚度 ,HE和VG染色分别观察大鼠心肌细胞和间质胶原纤维的变化 ,免疫组化检测血管紧张素Ⅱ及其I型受体表达水平。结果 扩张型心肌病大鼠左室收缩功能下降 ;左心室内径增大、游离壁变薄 ;心肌细胞肥大、变性 ,核增大、分裂、畸形 ,间质胶原纤维增生 ;左室心肌血管紧张素II表达水平升高 ,而血管紧张素III型受体表达水平降低。结论 血管紧张素II水平升高可能是呋喃唑酮扩张型心肌病大鼠心室间纤维化的原因之一。
Objectives To explore the role of angiotensin Ⅱ and it's type I receptor in ventricular collagen network remodeling in rats with dilated cardiomyopathy.Methods The model of dilated cardiomyopathy was created in wistar rats by fed with furazolidone. The cardiac function of rat was detected by echocardiography. Left ventricular interior diameter and the thickness of ventricular free wall were measured after the rats were killed. Myocardial cell morphology and interstitial collagen was observed by HE and V-G stain. Angiotensin Ⅱand it's type I receptor were measured by immunohistochemical method.Results In the dilated cardiomyopathy group, the cardiac function was decreased, the left ventricular interior diameter became wide and the thickness of ventricular free was thin, cardiac myocyte hypertrophy and lysis accompanied with nucleus augmentation, differentiation and deformation, the interstitial collagen fibers were increased, the level of angiotensin Ⅱ was increased, but the level of type I receptor was decreased.Conclusions The upregulation of angiotensin Ⅱ level may be one of the reasons of fibrosis in ventricular interstitial collagen of rats with furazolidone-induced dilated cardiomyopathy.
出处
《岭南心血管病杂志》
2004年第4期299-301,共3页
South China Journal of Cardiovascular Diseases
