title: Myocardial contractile dysfunction contributes to the development of heart failure in rats with aortic stenosis.
abstract: OBJECTIVE
  To analyze the potential contribution of contractility state and ventricular geometry to the development of heart failure in rats with aortic stenosis.
  
  
  METHODS
  Rats were divided into three groups: compensated aortic stenosis (AS, n=11), heart failure AS (n=12) and control rats (C, n=13).
  
  
  RESULTS
  After 21 weeks, failing AS rats presented higher systolic (C=36.6+/-3.1, AS=78.6+/-4.8*, failing AS=104.6+/-7.8*(dagger)) and diastolic meridian stress (C=6.9+/-0.4, AS=20.1+/-1.1*, failing AS=43.2+/-3.2*(dagger)), hydroxyproline (C=3.6+/-0.7 mg/g, AS=6.6+/-0.6* mg/g, failing AS=9.2+/-1.4*(dagger) mg/g) and cross-sectional area (C=338+/-25 microm2, AS=451+/-32* microm2, failing AS=508+/-36*(dagger) microm2), in comparison with control and compensated AS animals (*p<0.05 vs. control, (dagger)p<0.05 vs. AS). In the isometric contraction study, considering the time from peak tension to 50% relaxation (RT50), the relative variation responses, following post-rest contraction and increase in Ca2+ concentration, were higher in failing AS than compensated AS animals. In contrast, following post-rest contraction, compensated AS group presented higher values of the peak developed tension (DT) than failing AS group. Following beta-adrenergic stimulation, control animals presented higher values of +dT/dt and -dT/dt than AS animals. In addition, failing AS animals presented higher TPT values than compensated AS animals.
  
  
  CONCLUSIONS
  Myocardial contractile dysfunction contributes to the development of heart failure in rats with aortic stenosis.
authors.affiliation: Departamento de Clínica Médica, Faculdade de Medicina de Botucatu, Universidade Estadual Paulista, Botucatu, São Paulo, 18618-000, Brazil.
authors.forename: Edson A
authors.initials: EA
authors.lastname: Bregagnollo
authors.forename: Leonardo A M
authors.initials: LA
authors.lastname: Zornoff
authors.forename: Katashi
authors.initials: K
authors.lastname: Okoshi
authors.forename: Mario
authors.initials: M
authors.lastname: Sugizaki
authors.forename: Marco A
authors.initials: MA
authors.lastname: Mestrinel
authors.forename: Carlos R
authors.initials: CR
authors.lastname: Padovani
authors.forename: Antonio C
authors.initials: AC
authors.lastname: Cicogna
mesh_terms: D000818:Animals; D001024:Aortic Valve Stenosis / Q000150:complications* / Q000503:physiopathology*; D001794:Blood Pressure; D004195:Disease Models, Animal; D006333:Heart Failure / Q000209:etiology* / Q000503:physiopathology*; D006339:Heart Rate; D008297:Male; D009200:Myocardial Contraction; D010210:Papillary Muscles / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D012016:Reference Values; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000000981:diagnostic imaging; D020257:Ventricular Remodeling