Left ventricular failure induced by myocardial infarction. II. Tissue morphometry.
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.
Anversa
P
P
Loud
A V
AV
Levicky
V
V
Guideri
G
G
D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000818:Animals; D006332:Cardiomegaly / Q000209:etiology*; D003326:Coronary Circulation; D005109:Extracellular Matrix / Q000473:pathology; D006321:Heart / Q000503:physiopathology*; D008297:Male; D008433:Mathematics; D009203:Myocardial Infarction / Q000150:complications / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology*; D010101:Oxygen Consumption; D051381:Rats; D011919:Rats, Inbred Strains
D000255:Adenosine Triphosphate