Myocardial Infarction in Rats: Infarct Size, Myocyte Hypertrophy, and Capillary Growth

• Published in: Circulation research Vol. 58; no. 1; pp. 26 - 37
• Main Authors: Anversa, Piero, Beghi, Cesare, Kikkawa, Yutaka, Olivetti, Giorgio
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD American Heart Association, Inc 01.01.1986; Lippincott
• Subjects: Animals; Biological and medical sciences; Capillaries - pathology; Cardiology. Vascular system; Cell Nucleus - pathology; Coronary heart disease; Coronary Vessels - pathology; Cytoplasm - pathology; Heart; Hypertrophy; Male; Medical sciences; Mitochondria - pathology; Myocardial Infarction - pathology; Myocardium - pathology; Organ Size; Rats; Rats, Inbred WKY; Heart; Infarct; Rat; Growth; Rodentia; Cardiovascular disease; Electron microscopy; Coronary heart disease; Myocyte; Pathology; Vertebrata; Experimental disease; Mammalia; Myocardium; Blood capillary; Hypertrophy
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.res.58.1.26

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