AJP - Heart and Circulatory Physiology, Vol 248, Issue 6 883-H889, Copyright © 1985 by American Physiological Society
Left ventricular failure induced by myocardial infarction. II. Tissue morphometry
P. Anversa, A. V. Loud, V. Levicky and G. Guideri
Three days after myocardial infarction involving 57% of the left ventricle
in rats, the viable tissue of the left ventricle expanded 29%, whereas
myocardial hypertrophy in the right ventricle was 19%. To determine whether
tissue oxygenation in the hypertrophied ventricles was supported by a
proportional growth of the capillary network, morphometric analysis was
used to measure capillary luminal volume and surface densities and the
diffusion distance for O2. The volume fraction of capillary lumen and the
luminal surface of capillaries, related to O2 availability and diffusion,
were altered by -21 and -19%, respectively, in the left ventricle and by
-23 and -20%, respectively, in the right ventricle. The path length for O2
transport was found to be increased by 12 and 15% in the left and right
ventricle, respectively. In contrast, myocyte mass expanded in proportion
to tissue growth in the left ventricle and exceeded tissue growth by 5% in
the right ventricle. Myocyte mitochondria and myofibrils both grew in
proportion to the cells, so that their volume ratio was not changed in
either ventricle. The relatively inadequate adaptation of the capillary
vasculature suggests that hypertrophy after severe myocardial infarction
may initially leave the heart more vulnerable to additional ischemic
episodes.
