M. Gerova et al., REMODELING AND FUNCTIONAL ALTERATIONS OF THE RABBIT CORONARY-ARTERY IN VOLUME-OVERLOADED HEART, Cardiovascular Research, 27(11), 1993, pp. 2005-2010
Objective: The aim was to study the contractility of the conduit coron
ary artery to vasoactive agents in developing and established volume o
verload cardiac hypertrophy and to compare it with structural alterati
ons in the artery. Methods: Aortic valve insufficiency in rabbits was
used to produce a volume overloaded heart. One month (developing hyper
trophy), and four months (stabilised hypertrophy) after inducing aorti
c insufficiency, the isometric contraction of the coronary artery to a
cetylcholine, serotonin, and potassium chloride was recorded. For tran
smission electron microscopy, the coronary arteries were perfused via
the ascending aorta with glutaraldehyde fixative under constant pressu
re. The point counting method was used for quantitative evaluation. Se
mithin sections were used to determine the geometry (ie, the inner dia
meter and wall thickness) of the coronary artery by light microscopy.
Results: A significant increase in heart weight and heart weight to bo
dy weight ratio was found after one month and four months of volume ov
erload. 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 significa
nt. The contractions were weakened by up to one fifth of the control v
alues. 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 f
indings (an increase of the area occupied by organelles in myocytes) s
uggested a transition from ''contractile'' to more ''synthetic'' type
of smooth muscle cells. Conclusions: In cardiac hypertrophy due to vol
ume overload, the structure of the coronary arteries reflects the long
term haemodynamic alterations, particularly through an increase in th
e non-cellular component. In parallel, the contraction efficiency to v
asoactive drugs decreases markedly.