Inhibition of Protein Synthesis in Cardiac Hypertrophy and its Relation to Myocardial Failure
The rate of myocardial protein synthesis was studied in hearts of rabbits with experimentally produced cardiac hypertrophy and treatment with actinomycin D and puromycin as well as in animals maintained on a protein-free diet. Actinomycin D and puromycin inhibited myocardial incorporation of glycine-2-C14 only if protein synthesis was stimulated by means of aortic stenosis. Actinomycin D had no effect on the normal myocardium. Animals on protein-free diet also showed a decreased rate of glycine-2-C14 uptake into heart muscle protein after production of aortic stenosis, but an increased incorporation into skeletal muscle protein. Inhibition of protein synthesis during the first stage of cardiac hypertrophy was associated with the development of heart failure, regardless of whether the inhibition occurred as a result of actinomycin D, of puromycin or of protein-free diet. As compared to animals maintained on a regular diet, myocardial protein turnover rate in unoperated animals was not altered significantly by protein-free diet.
- Accepted November 12, 1965.
- © 1966 American Heart Association, Inc.