title: Structural and biomechanical alterations in rabbit thoracic aortas are associated with the progression of atherosclerosis.
abstract: BACKGROUND
  Atherosclerosis is a diffuse and highly variable disease of arteries that alters the mechanical properties of the vessel wall through highly variable changes in its cellular composition and histological structure. We have analyzed the effects of acute atherosclerotic changes on the mechanical properties of the descending thoracic aorta of rabbits fed a 4% cholesterol diet.
  
  
  METHODS
  Two groups of eight male New Zealand White rabbits were randomly selected and fed for 8 weeks either an atherogenic diet (4% cholesterol plus regular rabbit chow), or regular chow. Animals were sacrificed after 8 weeks, and the descending thoracic aortas were excised for pressure-diameter tests and histological evaluation to examine the relationship between aortic elastic properties and atherosclerotic lesions.
  
  
  RESULTS
  All rabbits fed the high-cholesterol diet developed either intermediate or advanced atherosclerotic lesions, particularly American Heart Association-type III and IV, which were fatty and contained abundant lipid-filled foam cells (RAM 11-positive cells) and fewer SMCs with solid-like actin staining (HHF-35-positive cells). In contrast, rabbits fed a normal diet had no visible atherosclerotic changes. The atherosclerotic lesions correlated with a statistically significant decrease in mean vessel wall stiffness in the cholesterol-fed rabbits (51.52 ± 8.76 kPa) compared to the control animals (68.98 ± 11.98 kPa), especially in rabbits with more progressive disease.
  
  
  CONCLUSIONS
  Notably, stiffness appears to decrease with the progression of atherosclerosis after the 8-week period.
authors.affiliation: Cardiothoracic Surgery Department, University Hospital of Patras, Patras, Greece. iokoniari@yahoo.gr
authors.forename: Ioanna
authors.initials: I
authors.lastname: Koniari
authors.forename: Dimosthenis
authors.initials: D
authors.lastname: Mavrilas
authors.forename: Helen
authors.initials: H
authors.lastname: Papadaki
authors.forename: Menelaos
authors.initials: M
authors.lastname: Karanikolas
authors.forename: Martha
authors.initials: M
authors.lastname: Mandellou
authors.forename: Apostolos
authors.initials: A
authors.lastname: Papalois
authors.forename: Efstratios
authors.initials: E
authors.lastname: Koletsis
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Dougenis
authors.forename: Efstratios
authors.initials: E
authors.lastname: Apostolakis
mesh_terms: D000465:Algorithms; D000818:Animals; D001013:Aorta, Thoracic / Q000473:pathology* / Q000503:physiopathology; D050197:Atherosclerosis / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D001696:Biomechanical Phenomena; D002784:Cholesterol / Q000009:adverse effects; D004108:Dilatation, Pathologic; D005487:Foam Cells / Q000378:metabolism / Q000473:pathology; D006937:Hypercholesterolemia / Q000139:chemically induced / Q000150:complications; D066298:In Vitro Techniques; D008297:Male; D032389:Myocytes, Smooth Muscle / Q000378:metabolism / Q000473:pathology; D011817:Rabbits
chemical_list: D002784:Cholesterol