@entity583 in @entity35 . Infarct size, myocyte XXXX , and capillary growth.

@entity39 @entity1184 @entity1283 @entity63 @entity1188 @entity35 @entity583
To determine the compensatory reserve capacity of the ventricular myocardium following infarction, the left coronary artery in @entity35 was ligated, and the animals were killed 40 days later. @entity1188 affecting an average 23% of the left ventricle were characterized by a 27% @entity1184 growth of the remaining myocardium that produced a complete replacement of the @entity39 tissue. In contrast, @entity1188 with an average 50% loss of mass resulted in 83% expansion of the spared myocardium that was inadequate for a complete restoration of ventricular tissue. Myocyte @entity1184 was 26% and 78% in small and large @entity1188 , respectively. Cellular @entity1184 in both cases involved significant increases in myocyte transverse area and myocyte length. After large @entity1188 , there was an 18% reduction in capillary surface and a 16% increase in the diffusion distance. Corresponding values for small @entity1188 were -10% and 9%. These alterations combined with the deficient reconstitution of myocardial mass following large @entity1188 resulted in 25%, 29%, and 30% deficits in the absolute amounts of capillary lumen, surface, and length per ventricle respectively. Even with small @entity1188 , a deficit was seen in capillary luminal surface (-16%), and length (-19%). In conclusion, we have demonstrated that @entity1283 following @entity583 is consistent with cellular shape changes characteristic of a combination of concentric and eccentric @entity1184 growth. However, cardiac muscle cells appear to be unable to compensate for the loss of mass induced by a 50% @entity1188 . The inadequate adaptation of the capillary vasculature in the infarcted hearts suggests that the injured ventricle is more vulnerable to additional @entity63 episodes.
