AJP - Heart and Circulatory Physiology, Vol 251, Issue 3 664-H669, Copyright © 1986 by American Physiological Society
Myocardial mechanics in allylamine-induced myocardial fibrosis
Y. Nakamura, A. W. Wiegner, J. T. Aslanis, C. S. Apstein and O. H. Bing
To examine the effect of fibrosis on myocardial mechanics, we studied
isolated left ventricular papillary muscles from 18 rats given 0.1%
allylamine, an agent known to cause myocardial fibrosis, in drinking water
for 4-8 wk. Six control rats were given tap water. Left ventricular
hydroxyproline concentration was higher in the allylamine-treated group
[3.47 +/- 2.12 vs. 2.10 +/- 0.66 (SD) micrograms/mg dry wt; P less than
0.01]. Because of variable and heterogeneous involvement of the ventricle
by fibrosis, preparations from allylamine-fed rats were divided into two
subgroups; data from four papillary muscles with more than 25% fibrosis by
point counting (AL-B group) were compared with eight control muscles from
nonallylamine-treated rats. A third subgroup of nine muscles from
allylamine-treated rats but with normal left ventricular hydroxyproline
concentration and fibrosis as determined by point counting served as
another control group (AL-A) for the evaluation of effects of allylamine
not due to fibrosis. Myocardial fiber diameters of AL-B preparations were
significantly larger than other groups (controls, 12.1 +/- 1.7 microns;
AL-A group, 12.7 +/- 1.7 microns; AL-B group, 18.0 +/- 1.2 microns; P less
than 0.01). Passive and active stiffness constants in AL-B muscles were
significantly increased compared with control and AL-A preparations (P less
than 0.05). Electromechanical delay plus time to peak tension and the time
for tension to fall from its peak to one-half of that value at the peak of
the length-tension curve were significantly prolonged in AL-B
muscles.(ABSTRACT TRUNCATED AT 250 WORDS)
