Morphometric analysis of coronary capillaries during physiologic myocardial growth and induced cardiac hypertrophy: a review.
The quantitative structural properties of the ventricular myocardium with respect to its capillary concentration and distribution have been measured morphometrically during postnatal physiologic growth and later in life in the rat, and compared with those accompanying an increased load in the adult heart to determine whether induced cardiac hypertrophy is a pathologic condition or a form of accelerated myocardial growth. The following morphometric parameters of the capillary microvasculature were examined: 1. Capillary luminal volume density; 2. Capillary luminal surface density; and 3. The average diffusion distance for oxygen. The expansion of the ventricular myocardium during maturation shows a remarkable degree of well balanced compensatory response, because the capillary microvasculature and myocytes grow in proportion to the increase in cardiac mass. In older rats parenchymal cells increase more than the capillary network resulting in a reduction of the oxygenation potential of the tissue and local ischemic damage. Cardiac hypertrophy produced by pressure overload, volume overload and by a combination of both may also show alterations affecting capillary luminal volume and surface densities and the path length for oxygen molecular transport, which indicate an inadequate growth adaption of the component structures responsible for tissue oxygenation. In conclusion, myocardial enlargement that develops with age or as a result of an increased work load on the heart may lead to a conditioned state of the myocardium that can be expected to increase its vulnerability to ischemia as in pathologic cardiac hypertrophy.
Anversa
P
P
Department of Pathology, New York Medical College, Valhalla.
Capasso
J M
JM
Ricci
R
R
Sonnenblick
E H
EH
Olivetti
G
G
D000375:Aging; D000818:Animals; D002196:Capillaries / Q000648:ultrastructure*; D006332:Cardiomegaly / Q000503:physiopathology; D003331:Coronary Vessels / Q000648:ultrastructure*; D006321:Heart / Q000502:physiology; D008833:Microcirculation / Q000502:physiology; D009206:Myocardium / Q000166:cytology; D051381:Rats