Inhibition of protein synthesis in cardiac hypertrophy and its relation to myocardial failure.

• It has been demonstrated that a heart subjected to functional strain, imposed by increased outflow resistance, passes through a series of metabolic alterations, characterized by changes in energy production and myocardial protein synthesis. Under such circumstances an isometric type of hyperfunction is produced with the development of cardiac hypertrophy. During the first or "damage" stage of hyperfunction, which occurs immediately after severe outflow obstruction protein synthesis is increased; during the second stage of relatively stable hyperfunction the degree of protein synthesis approaches normal levels, while during the third stage, which is characterized functionally by gradual exhaustion, protein synthesis is inhibited. It was postulated that the primary inhibition of protein synthesis interferes with the renewal of the energy-producing and contractile structures of the myocardium. This results in a disturbance in the processes of energy production and utilization with a decrease in the contractile capacity of the myocardium.Previous experiments in this laboratory' have shown that in cardiac hypertrophy protein synthesis is increased but there is no increase in myocardial protein turnover rate. It is the purpose of this study to investigate the relationship between cardiac hypertrophy