title: [Study of effects of drugs on myocardial hypertrophy due to overload].
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Cardiology, Changzhi People's Hospital, Changzhi 046000, Shanxi, China.
authors.forename: Guo-ping
authors.initials: GP
authors.lastname: Wang
authors.forename: Rong-hui
authors.initials: RH
authors.lastname: Cao
authors.forename: Yong-gang
authors.initials: YG
authors.lastname: Du
authors.forename: Zi-yan
authors.initials: ZY
authors.lastname: Zhang
authors.forename: Ji-yuan
authors.initials: JY
authors.lastname: Lü
authors.forename: Shu-lan
authors.initials: SL
authors.lastname: Chen
authors.forename: Zhong-dong
authors.initials: ZD
authors.lastname: Qiao
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000804:Angiotensin II / Q000378:metabolism*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000378:metabolism; D000818:Animals; D002227:Carbazoles / Q000627:therapeutic use; D004195:Disease Models, Animal; D019332:Endothelin-1 / Q000378:metabolism*; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D048289:Imidazolidines / Q000627:therapeutic use*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D011412:Propanolamines / Q000627:therapeutic use; D011897:Random Allocation; D051381:Rats; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D002227:Carbazoles; D019332:Endothelin-1; D048289:Imidazolidines; D011412:Propanolamines; D014409:Tumor Necrosis Factor-alpha; D000804:Angiotensin II; C065166:imidapril