Furazolidone induces dilated cardiomyopathy in rats
- VernacularTitle:呋喃唑酮制备大鼠扩张型心肌病模型
- Author:
Rongjie HUANG
;
Tangwei LIU
;
Weifeng WU
;
Yusheng PANG
- Publication Type:Journal Article
- Keywords:
Furazolidone;
Cardiomyopathy, congestive;
Animal model
- From:
Chinese Journal of Pathophysiology
2000;0(11):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To establish the Wistar rat model of furazolidone-induced dilated cardiomyopathy (Fz-DCM). METHODS: The Wistar rat model of Fz-DCM was established by feeding the animals with furazolidone. The left ventricular dimension and cardiac function were detected by echocardiogram. Aortic and right atrial pressure were measured by invasive catheter. Left ventricular interior diameter and the thickness of left ventricular free wall were measured after the rats were killed. Myocardial collagen network remodeling was observed and collagen volume fraction (CVF) was calculated by Van Gieson stain. RESULTS: ①The total incidence rate of DCM was 66.6% (20/30) in DCM group. ②Compared the corresponding subgroups to control group, the left ventricular end-diastolic diameter (LVED), left ventricular end-systolic diameter (LVES), the right atrial pressure, the left ventricular interior diameter and the ratio of left ventricle weight and body weight were increased significantly. The fraction shortening (FS), the left ventricular ejection fraction (LVEF) and the thickness of left ventricular free wall were decreased significantly. ③In FZ-DCM rat, the myocyte hypertrophy and degeneration, interistial fibrous tissue hyperplasia, the quantity of typeⅠand type Ⅲ collagen fibers and the collagen volume fraction (CVF%) were increased significantly. CONCLUSIONS: The rat model of DCM can be induced successfully by feeding the animals with furazolidone. In the rats with Fz-DCM, there are left ventricular dilation, the thinness of ventricular wall, the interistial fibrous tissue hyperplasia, and the decrease in left ventricular contractic function, indicating that the Fz-DCM rat model represents the pathophysiological characters of dilated cardiomyopathy.
