title: A mouse model of reverse cardiac remodelling following banding-debanding of the ascending aorta.
abstract: OBJECTIVE
  Myocardial remodelling during pressure overload might contribute to development of heart failure. Reverse remodelling normally occurs following aortic valve replacement for aortic stenosis; however, the details and regulatory mechanisms of reverse remodelling remain unknown. Thus, an experimental model of reverse remodelling would allow for studies of this process. Although models of aortic banding are widely used, only few reports of debanding models exist. The aim of this study was to establish a banding-debanding model in the mouse with repetitive careful haemodynamic evaluation by high-resolution echocardiography.
  
  
  METHODS
  C57Bl/6 mice were subjected to ascending aortic banding and subsequent debanding. Cardiac geometry and function were evaluated by echocardiography, and left ventricular myocardium was analysed by histology and quantitative real-time polymerase chain reaction.
  
  
  RESULTS
  The degree of aortic banding was controlled by non-invasive estimation of the gradient, and we found a close correlation between left ventricular mass estimated by echocardiography and weight at the time of killing. Aortic banding led to left ventricular hypertrophy, fibrosis and expression of foetal genes, indicating myocardial remodelling. Echocardiography revealed concentric left ventricular remodelling and myocardial dysfunction. Following debanding, performed via a different incision, there was rapid regression of left ventricular weight and normalization of both cardiac geometry and function by 14 days.
  
  
  CONCLUSIONS
  We have established a reproducible and carefully characterized mouse model of reverse remodelling by banding and debanding of the ascending aorta. Such a model might contribute to increased understanding of the reversibility of cardiac pathology, which in turn might give rise to new strategies in heart failure treatment.
authors.affiliation: Department of Cardiothoracic Surgery, Oslo University Hospital Ullevål, Norway. j.l.bjornstad@medisin.uio.no
authors.forename: J L
authors.initials: JL
authors.lastname: Bjørnstad
authors.forename: B
authors.initials: B
authors.lastname: Skrbic
authors.forename: I
authors.initials: I
authors.lastname: Sjaastad
authors.forename: S
authors.initials: S
authors.lastname: Bjørnstad
authors.forename: G
authors.initials: G
authors.lastname: Christensen
authors.forename: T
authors.initials: T
authors.lastname: Tønnessen
mesh_terms: D000818:Animals; D001011:Aorta / Q000000981:diagnostic imaging / Q000503:physiopathology*; D004195:Disease Models, Animal; D006321:Heart / Q000503:physiopathology; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D051379:Mice; D009206:Myocardium / Q000473:pathology; D032383:Myocytes, Cardiac / Q000000981:diagnostic imaging / Q000473:pathology / Q000502:physiology; D014463:Ultrasonography; D020257:Ventricular Remodeling / Q000502:physiology*