The surviving myocardium of the cat was studied 7 days and 6 weeks following experimental infarction.

Seven days after infarction, ultrastructural alterations of the mitochondria indicative of slight hypoxic injury—clearing of the matrix and loss of dense matrix granules-were found. Together with intracellular edema and glycogen depletion this result was considered as a sign of relative hypoxia in the surviving myocardium 7 days after infarction. At the same time β-glucuronidase activity of tissue homogennates was found to be elevated. Focal ischemic lesions in remote myocardium which have been described by other authors (5, 6, 23) were not detected in our experiments.

Six weeks after infarction, the fractional volume occupied by myofibrils had increased whereas the fractional volume of mitochondria had remained unchanged (left ventricle) resp. had decreased (right ventricle). There were no qualitative changes detectable at the ultrastructural level. Based on the morphometric investigation of Anversa (1, 2), our results were regarded indicative of mild compensatory hypertrophy of the surviving myocardium. Glutamate dehydrogenase activity of tissue homogenates was shown to be increased when compared to control values.

Furthermore our morphometric results showed that the unit mass of mitochondria has to render an enhanced amount of energy six weeks after infarction which might leave the surviving myocardium with a higher susceptibility to future hypoxic injury.