AJP - Heart and Circulatory Physiology, Vol 249, Issue 5 1031-H1037, Copyright © 1985 by American Physiological Society
Hypertrophy and coronary and collateral vascularity in dogs with severe chronic anemia
K. W. Scheel and S. E. Williams
The purpose of this study was to determine 1) whether a severe hypoxic
stimulus could produce an increase in coronary and collateral
vascularization and 2) whether minimal coronary resistance, which increases
with hypertension-induced hypertrophy, decreases when hypoxia is
superimposed on volume load hypertrophy. Data were obtained on 11 dogs
rendered anemic to a hematocrit of 11 +/- 0.2 vol% and maintained at this
level for 4 wk. Eighteen dogs with a hematocrit of 42 +/- 0.02 vol% were
used as controls. After chronic anemia the coronary and collateral flows
were quantitated in a beating, vasodilated, isolated heart preparation
perfused solely with blood from two normal donor dogs. The following
variables were significantly increased in anemia-exposed hearts compared
with controls: coronary flow per gram myocardium for the left anterior
descending, the circumflex, the right, and the septal arteries; ratio of
total coronary flow of each vessel to body weight; and the collateral flows
to each coronary vessel. Both the right and left ventricles were
hypertrophied. We conclude that severe chronic anemia produces a
dissociation between hypertrophy and increased minimal coronary resistance.
Severe chronic anemia appears to increase vascularization of both coronary
and collateral circulation probably due to tissue hypoxia. In this model
coronary collateral vascularity seems to increase in the absence of a
pressure difference across collaterals.
