Regression of cardiac hypertrophy after closing an aortocaval
fistula in rats.
Gerdes, A. Martin, Linda C. Clark, and Joseph M. Capasso.
Department of Anatomy and Structural Biology, University of South
Dakota School of Medicine, Vermillion, South Dakota 57069.
APStracts 2:0023H, 1995.
To determine whether the series addition of sarcomeres observed during
eccentric hypertrophic growth is reversible upon removal of the
initiation stimulus, aortocaval fistula was created and myocyte
geometry evaluated at two and twelve weeks after shunt occlusion. One
month after creation of an aortocaval fistula in rats was associated
with a 76% cardiac enlargement which was reduced to 22% and 18% at 2
and 12 weeks of fistula reversal, respectively. Hemodynamic
performance was altered as a result of fistula induction as evidenced
by a 28% increase in peak rate of pressure rise which remained
elevated by 30% two weeks after fistula reversal but was not
different from sham-operated control animals at twelve weeks of
reversal. Significant increases in overall myocyte length were
detected as a result of the creation of the fistula (LV, 20%; RV,
29%; Septum, 23% greater than shams). Although these increases
diminished only slightly two weeks after closure of the fistula (LV,
12%; RV, 17%; Septum, 12% greater than shams), linear measurements of
myocyte length had reverted to values which were not significantly
different from those of age-matched sham operated controls at twelve
weeks after fistula closure (LV, 8%; RV, 10%; Septum, 7%). Myocyte
cross-sectional area and cell volume followed a similar pattern.
Thus, myocytes possess the necessary machinery to remove recently
added series sarcomeres, returning altered pump function and dilated
ventricular chamber geometry towards control values. In addition, it
appears that cardiac hypertrophic growth with this experimental model
of volume overload is largely, but not completely, reversible.
Received 12 August 1994; accepted in final form 11 January 1995.
APS Manuscript Number H725-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 24 February 1995.