title: Effect of testosterone on post-myocardial infarction remodeling and function.
abstract: BACKGROUND
  Men and women are differently affected by coronary artery disease, suggesting an important role of sex steroids. Moreover, testosterone (T) treatment is increasingly used in elderly males. Therefore, we examined effects of chronic anabolic T administration on left ventricular (LV) remodeling after myocardial infarction (MI).
  
  
  METHODS
  Adult male rats were treated with intramuscular placebo, testosterone undecanoate (T), or were orchiectomized. After 2 weeks, animals underwent sham-operation (sham) or left coronary artery ligation. Left ventricular remodeling and function was assessed by serial magnetic resonance imaging (MRI) at weeks 2 and 8 and hemodynamic investigation at week 8.
  
  
  RESULTS
  In sham operated animals T administration increased serum T levels and led to cardiac hypertrophy, but not to an upregulation of ANP mRNA. The alpha/beta-MHC ratio was significantly higher after T treatment due to an increase in alpha-MHC. As a potential mechanism for this "physiologic" form of hypertrophy, IGF-1 mRNA expression was significantly increased in T treated animals. After coronary artery ligation, infarct size and mortality were similar among the groups. Left ventricular hypertrophy was enhanced by T treatment. However, in vivo LV end-diastolic pressure and wall stress were decreased by T, whereas other hemodynamic parameters (mean arterial pressure, cardiac output, etc.) remained unchanged.
  
  
  CONCLUSIONS
  Chronic anabolic T treatment led to a specific "physiologic" pattern of myocardial hypertrophy with a significant increase in LV weight, but without differences in ANP and with an upregulation in alpha/beta-MHC, possibly mediated by IGF-1. Testosterone treatment had no detrimental effects following MI. Reduced wall stress and LVEDP may even improve long-term outcome.
authors.affiliation: Medical University Hospital Wuerzburg, Josef-Schneider-Strasse 2, 97080 Wuerzburg, Germany.
authors.forename: Matthias
authors.initials: M
authors.lastname: Nahrendorf
authors.forename: Stefan
authors.initials: S
authors.lastname: Frantz
authors.forename: Kai
authors.initials: K
authors.lastname: Hu
authors.forename: Constantin
authors.initials: C
authors.lastname: von zur Mühlen
authors.forename: Maria
authors.initials: M
authors.lastname: Tomaszewski
authors.forename: Heidi
authors.initials: H
authors.lastname: Scheuermann
authors.forename: Ralf
authors.initials: R
authors.lastname: Kaiser
authors.forename: Virginija
authors.initials: V
authors.lastname: Jazbutyte
authors.forename: Stephanie
authors.initials: S
authors.lastname: Beer
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Bauer
authors.forename: Stefan
authors.initials: S
authors.lastname: Neubauer
authors.forename: Georg
authors.initials: G
authors.lastname: Ertl
authors.forename: Bruno
authors.initials: B
authors.lastname: Allolio
authors.forename: Frank
authors.initials: F
authors.lastname: Callies
mesh_terms: D000818:Animals; D005786:Gene Expression Regulation / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D017379:Hypertrophy, Left Ventricular / Q000139:chemically induced; D007334:Insulin-Like Growth Factor I / Q000096:biosynthesis / Q000235:genetics; D019028:Magnetic Resonance Imaging, Cine / Q000379:methods; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism / Q000503:physiopathology*; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D013739:Testosterone / Q000031:analogs & derivatives* / Q000097:blood / Q000494:pharmacology*; D020257:Ventricular Remodeling / Q000187:drug effects*
chemical_list: D012333:RNA, Messenger; D013739:Testosterone; D007334:Insulin-Like Growth Factor I; C010792:testosterone undecanoate