title: Remodelling and functional alterations of the rabbit coronary artery in volume overloaded heart.
abstract: OBJECTIVE
  The aim was to study the contractility of the conduit coronary artery to vasoactive agents in developing and established volume overload cardiac hypertrophy and to compare it with structural alterations in the artery.
  
  
  METHODS
  Aortic valve insufficiency in rabbits was used to produce a volume overloaded heart. One month (developing hypertrophy), and four months (stabilised hypertrophy) after inducing aortic insufficiency, the isometric contraction of the coronary artery to acetylcholine, serotonin, and potassium chloride was recorded. For transmission electron microscopy, the coronary arteries were perfused via the ascending aorta with glutaraldehyde fixative under constant pressure. The point counting method was used for quantitative evaluation. Semithin sections were used to determine the geometry (ie, the inner diameter and wall thickness) of the coronary artery by light microscopy.
  
  
  RESULTS
  A significant increase in heart weight and heart weight to body weight ratio was found after one month and four months of volume overload. Concentration-response relations of the coronary artery to all three agents were shifted to the right; in developing hypertrophy the shift was non-significant, in stabilised hypertrophy it was significant. The contractions were weakened by up to one fifth of the control values. An associated increase in wall thickness of the coronary artery was found, due to a significant expansion of the intercellular space. The internal diameter did not change significantly. Ultrastructural findings (an increase of the area occupied by organelles in myocytes) suggested a transition from "contractile" to more "synthetic" type of smooth muscle cells.
  
  
  CONCLUSIONS
  In cardiac hypertrophy due to volume overload, the structure of the coronary arteries reflects the long term haemodynamic alterations, particularly through an increase in the non-cellular component. In parallel, the contraction efficiency to vasoactive drugs decreases markedly.
authors.affiliation: Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava.
authors.forename: M
authors.initials: M
authors.lastname: Gerová
authors.forename: A
authors.initials: A
authors.lastname: Holécyová
authors.forename: F
authors.initials: F
authors.lastname: Kristek
authors.forename: A
authors.initials: A
authors.lastname: Fízel'
authors.forename: A
authors.initials: A
authors.lastname: Fízel'ová
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D006332:Cardiomegaly / Q000473:pathology / Q000503:physiopathology*; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology* / Q000648:ultrastructure; D005260:Female; D008297:Male; D008854:Microscopy, Electron; D011189:Potassium Chloride / Q000494:pharmacology; D011817:Rabbits; D012701:Serotonin / Q000494:pharmacology; D017540:Tunica Media / Q000648:ultrastructure
chemical_list: D012701:Serotonin; D011189:Potassium Chloride; D000109:Acetylcholine