Wang Guo-ping, Cao Rong-hui, Du Yong-gang, Zhang Zi-yan, Lü Ji-yuan, Chen Shu-lan, Qiao Zhong-dong
Department of Cardiology, Changzhi People's Hospital, Changzhi 046000, Shanxi, China.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2005 Nov;17(11):670-2.
To study the relation of expression change of tumor necrosis factor-alpha (TNF-alpha), angiotensin II (Ang II), and endothelin-1 (ET-1), and the effect of imidapril on myocardial hypertrophy due to overload.
Sixty-three rats were randomly divided into four groups: sham operation (n=15), overload group (n=16), imidapril group (n=16), and Caweidiluo group (n=16). Hypertrophic myocardium was reproduced in rats by constricting abdominal aorta. Blood samples and heart were harvested 12 weeks after aorta constriction, and myocardial hypertrophy index, the contents of Ang II, ET-1 in the myocardium and plasma were determined by radioimmunoassay and TNF-alpha in the myocardium and plasma were determined by enzyme linked immunoadsorbent assay.
Left ventricle showed obvious hypertrophy 12 weeks after operation. The contents of TNF-alpha, Ang II and ET-1 in the myocardium, and the content of TNF-alpha in serum, Ang II and ET-1 in plasma were increased compared with those of controls (all P<0.01). The treatment of imidapril and Caweidiluo could restrain the development of left ventricle hypertrophy after operation, and imidapril decreased the contents of TNF-alpha, Ang II and ET-1 in myocardium compared with overload group (all P<0.01). Imidapril lowered the contents of TNF-alpha in serum, Ang II and ET-1 in plasma, compared with overload group (all P<0.01), but not ET-1. Caweidiluo lowered the contents of TNF-alpha, Ang II and ET-1 in myocardium, the contents of TNF-alpha in serum, Ang II and ET-1 in plasma (all P<0.01) compared with overload group (both P<0.01).
The activation of rennin-angiotensin system (RAS) by over load results to an elevation of TNF-alpha contents in plasma and myocardium, and it is probably one of the major regulatory pathways of myocardial hypertrophy.
研究肿瘤坏死因子-α（TNF-α）、血管紧张素II（Ang II）和内皮素-1（ET-1）表达变化的关系，以及咪达普利对负荷过重所致心肌肥厚的影响。
63只大鼠随机分为四组：假手术组（n=15）、负荷过重组（n=16）、咪达普利组（n=16）和卡维地洛组（n=16）。通过缩窄腹主动脉在大鼠中复制肥厚心肌。主动脉缩窄12周后采集血样和心脏，采用放射免疫法测定心肌肥厚指数、心肌和血浆中Ang II、ET-1的含量，采用酶联免疫吸附测定法测定心肌和血浆中TNF-α的含量。
术后12周左心室出现明显肥厚。与对照组相比，心肌中TNF-α、Ang II和ET-1的含量以及血清中TNF-α的含量、血浆中Ang II和ET-1的含量均升高（均P<0.01）。咪达普利和卡维地洛治疗可抑制术后左心室肥厚的发展，与负荷过重组相比，咪达普利降低了心肌中TNF-α、Ang II和ET-1的含量（均P<0.01）。与负荷过重组相比，咪达普利降低了血清中TNF-α的含量、血浆中Ang II和ET-1的含量（均P<0.01），但对ET-1无影响。与负荷过重组相比，卡维地洛降低了心肌中TNF-α、Ang II和ET-1的含量，血清中TNF-α的含量，血浆中Ang II和ET-1的含量（均P<0.01）。
负荷过重激活肾素-血管紧张素系统（RAS）导致血浆和心肌中TNF-α含量升高，这可能是心肌肥厚的主要调节途径之一。
